Frenchkearney9917

121, respectively). Moreover, the median OS and RFS times of the BDTT patients who underwent tumour thrombectomy and bile duct resection were not significantly different (P=0.891 and P=0.787, respectively). In the multivariate analysis, macrovascular invasion (HR, 3.701; 95% CI, 1.313-9.10.437; P=0.013) was the only independent predictor of OS. Although the clinicopathological characteristics of the BDTT group suggested more advanced stage disease and poorer oncological outcomes than the group without BDTT, BDTT was not a poor prognostic factor for patients with HCC who underwent liver resection. Curative resection is recommended for patients with HCC and BDTT, even for those with poor liver function, after proper perioperative management in order to achieve good long-term survival.Cutaneous melanoma (CM) is the most aggressive form of skin cancer, exhibits an increasing incidence worldwide and has a high potential to develop metastasis. The current study aimed to identify a set of parameters that may aid in predicting the probability and timing of the onset of CM metastasis. A retrospective analysis was performed using the archive data of 2,026 patients with CM that were treated at the Riga East University Hospital Latvian Oncology Centre, which is the largest oncological hospital in the country, between 1998 and 2015. A case-control study design was employed, where patients with metastasis (n=278) were used as the cases and patients without metastasis were used as the controls. The present study examined the associations between metastasis and potential risk factors and constructed multivariate models of features that predicted metastasis using stepwise regression. Time until metastasis was analyzed using negative binomial regression models. The results of the present study indicated an increase in the number of melanomas that developed metastases during 1998-2015. Tumor Breslow thickness was demonstrated to be significantly larger in patients with metastasis compared with those without (P=0.012). The presence of ulceration significantly increased the risk of metastases [odds ratio (OR), 1.66; 95% CI, 1.07-2.59; P=0.033]. The absence of pigment in melanoma tissues was indicated to lead to a greater likelihood of metastasis (OR, 2.14; 95% CI, 1.10-4.19; P=0.035). Shorter times from diagnosis until the onset of metastases were observed in older patients (incident rate ratio (IRR), 6.85; 95% CI, 2.43-19.30; P=2.78×10-4), and a borderline significant association was observed in those with ulcerated tumors (IRR, 1.33; 95% CI, 0.98-1.80; P=0.064). Therefore, the main features associated with the development of melanoma metastasis in Latvia were indicated to be tumor ulceration, absence of pigment and Breslow thickness.Pectolinarigenin a plant secondary metabolite that has various biological effects, including the inhibition of melanogenesis and tumor growth. Melanoma has a high degree of malignancy, with rapid metastasis and severe drug resistance, explaining the need for new candidate drugs that inhibit tumor growth and metastasis. However, the pharmacological action and mechanism of pectolinarigenin on the growth and metastasis of melanoma remain elusive. Thus, the present study aimed to investigate the role of pectolinarigenin in melanoma cell proliferation, apoptosis, migration and invasion. Apoptotic and metastasis-associated proteins were analyzed using western blotting. The results demonstrated that pectolinarigenin treatment resulted in growth inhibition and apoptosis induction in melanoma cells, arising from the loss of mitochondrial transmembrane potential, reactive oxygen species and the altered expression of apoptosis-associated proteins. In addition, wound-healing and Transwell assays demonstrated the potential of pectolinarigenin to impair the migration and invasion of melanoma cells in accordance with the changes in the expression of the associated proteins. Therefore, the results of the present study suggested that pectolinarigenin may serve a pivotal role in promoting melanoma cell apoptosis and reducing metastasis, and may thus be a promising potential candidate for an anti-melanoma treatment strategy.Gastric cancer is a leading cause of cancer-associated deaths worldwide and is considered to be an age-related disease. In younger patients, gastric cancer is biologically more aggressive, and prognosis is worse compared with that in elderly patients. In the present case report, the whole genome and transcriptome was sequenced in a 26-year-old patient with gastric cancer who presented with gastric cancer-related symptoms and was admitted to the First Affiliated Anhui Medical Hospital (Hefei, China) in December 2016. In total, 9 germline and 4 somatic mutations were identified in the patient, and there were more deleterious sites in the germline mutated genes. Genes with somatic mutations, such as MUC2, MUC4, SLC8A2, and with structural variations, including CCND3, FGFR2 and FGFR3, were found to be differentially expressed. Cancer-associated pathways, such as the 'calcium signaling pathway', 'cGMP-PKG signaling pathway' and 'transcriptional mis-regulation' were also enriched at both the genomic and transcriptomic levels. The genes found to have germline (SFRP4), somatic (MUC2, MUC4, SLC8A2) mutations, or structural variations (CCND3, FGFR2 and FGFR3) were differentially expressed in the patient and could be promising precision therapy targets.Colorectal cancer (CRC) is the third leading cause of cancer-associated mortality. The present study aimed to investigate novel biomarkers to predict prognosis and provide a theoretical basis for studies of the pathogenesis and the development of therapies for CRC. The present study compared mRNA expression levels of patients with CRC with short- and long-term prognosis and of individuals with and without tumors in The Cancer Genome Atlas (TCGA) database. Differentially expressed genes (DEGs) were identified via volcano plot and Venn diagram analysis. Gene Ontology (GO) analysis and gene set enrichment analysis (GSEA) were performed to identify the functions of the DEGs, and the DEGs were further verified using clinical CRC samples. A total of 10 DEGs were identified as candidate genes using the TCGA database, and four DEGs [defensin β 4A (DEFB4A), hyaluronan binding protein 2 (HABP2), oleoyl-ACP hydrolase and TBC1 domain family member 3G] were associated with poor prognosis of patients with CRC. Two DEGs (DEFB4A and HABP2) were upregulated in tumor tissues of patients with CRC in the TCGA database. GO and GSEA analyses revealed that DEFB4A was highly associated with immunosuppression, participates in 'myeloid leukocyte differentiation', 'leukocyte proliferation' and 'positive regulation of leukocyte-mediated immunity', and was positively correlated with CD11b, CD14, CD45, CD163 and IL17A. Furthermore, DEFB4A expression was significantly upregulated in patients with large tumors, advanced cancer stage, lymph node metastasis and liver metastasis. Survival analysis revealed that DEFB4A upregulation was associated with poor prognosis. DEFB4A gene knockdown experiments demonstrated that DEF4BA promotes cell migration. These results indicated that DEFB4A potentially promotes tumor growth by regulating immunosuppressive activity and provided novel insights into the diagnosis and treatment of CRC.The diagnosis of squamous cell carcinoma requires the accurate classification of cervical squamous lesions in the ThinPrep cytologic test (TCT). It primarily relies on a pathologist's interpretation under a microscope. Deep convolutional neural networks (DCNN) have played an increasingly important role in digital pathology. However, they have not been applied to diverse datasets and externally validated. In the present study, a DCNN model based on VGG16 and an ensemble training strategy (ETS) based on 5-fold cross-validation was employed to automatically classify normal and abnormal cervical squamous cells from a multi-center dataset. First, we collected a dataset comprising 82 TCT samples from four hospitals and fine-tuned our model twice on the dataset with and without the ETS. Then, we compared the classifications obtained from the models with those provided by two skilled pathologists to discriminate the performance of the models in terms of classification accuracy and efficiency. Finally, paired sample t-tests were used to validate the consistency between the classification provided by the proposed methods and that of the pathologists. The results showed that ETS slightly, though not significantly, improved the classification accuracy compared with that of the pathologists P0=0.387>0.05 (DCNN without ETS vs. DCNN with ETS), P1=0.771>0.05 (DCNN with ETS vs. pathologist 1), P2=0.489>0.05 (DCNN with ETS vs. pathologist 2). The DCNN model was almost 6-fold faster than that of the pathologists. The accuracy of our automated scheme was similar to that of the pathologists, but a higher efficiency in the accurate identification of cervical squamous lesions was provided by the scheme. This result allows for wider and more efficient screening and may provide a replacement for pathologists in the future. Future research should address the viability of the practical implementation of such DCNN models in the laboratory setting.Our previous study found that hydrogen gas (H2) could efficiently inhibit lung cancer progression; however, the underlying mechanisms still remains to be elucidated. The present study aimed to explore the roles of H2 in lung cancer cell autophagy, and reveal the effects of autophagy on H2-mediated lung cancer cell apoptosis and the underlying mechanisms. The expression levels of proteins associated with cell apoptosis and autophagy were detected using western blot analysis. Cell autophagy was inhibited by 3-methyladenine treatment or Beclin1 downregulation, while rapamycin was used to induce autophagy. Cell growth and apoptosis were detected using the Cell Counting Kit-8 and flow cytometry assays, respectively. The results demonstrated that cell apoptosis and autophagy were significantly enhanced in the A549 and H1975 lung cancer cell lines treated with H2. However, autophagy enhancement weakened H2 roles in promoting cell apoptosis and vice versa. In addition, it was found that H2 treatment induced marked decreases in the protein expression levels of phosphorylated STAT3 and Bcl2, and overexpression of STAT3 abolished H2 roles in promoting cell apoptosis and autophagy. Overall, the present study revealed that H2 can promote lung cancer cell apoptosis and autophagy via inhibiting the activation of STAT3/Bcl2 signaling and suppression of autophagy can enhance H2 roles in promoting lung cancer cell apoptosis.Drug resistance leads to tumor relapse and further progression during chemotherapy in lung cancer. Close homolog of L1 (CHL1) has been identified as a tumor suppressor in most malignancies. However, to the best of our knowledge, whether CHL1 mediates chemoresistance remains unknown. The present study observed that CHL1 was significantly downregulated in cisplatin (DDP)-resistant cells (A549/DDP) and paclitaxel (PTX)-resistant cells (A549/PTX) compared with A549 cells. When treated with or without DDP and PTX, silencing of CHL1 in A549 cells promoted the cell survival rate and clone formation, and decreased apoptosis. Whereas overexpression of CHL1 in A549/DDP and A549/PTX cells impeded the cell survival and clone formation and promoted apoptosis. Additionally, CHL1 overexpression enhanced the chemosensitivity of A549/DDP cells to DDP in vivo. Notably, the chemoresistance induced by CHL1 depletion was reversed by the Akt inhibitor SC66 in A549 cells. The results of the present study demonstrated that CHL1 enhanced sensitivity of lung cancer cells by suppressing the Akt pathway, which suggested that CHL1 may be a potential target for overcoming chemoresistance in lung cancer.Chronic colorectal inflammation has been associated with colorectal cancer (CRC); however, its exact molecular mechanisms remain unclear. The present study aimed to investigate the effect of Toll-like receptor 9 (TLR9) on the development of colitis-associated CRC (CAC) through its regulation of the NF-κB signaling pathway. By using a CAC mouse model and immunohistochemistry, the present study discovered that the protein expression levels of TLR9 were gradually upregulated during the development of CRC. In addition, the expression levels of TLR9 were revealed to be positively correlated with NF-κB and Ki67 expression levels. In vitro, inhibiting TLR9 expression levels using chloroquine decreased the cell viability, proliferation and migration of the CRC cell line HT29, and further experiments indicated that this may occur through downregulating the expression levels of NF-κB, proliferating cell nuclear antigen and Bcl-xl. In conclusion, the findings of the present study suggested that TLR9 may serve an important role in the development of CAC by regulating NF-κB signaling.[This corrects the article DOI 10.3892/ol.2019.10040.].[This retracts the article DOI 10.3892/ol.2020.11397.].Breast cancer is a highly heterogeneous disease at the molecular level and >90% of mortalities are due to metastasis and its associated complications. The present study determined the impact of molecular subtypes on metastatic behavior and overall survival (OS) of patients with metastatic breast cancer. The influence of molecular subtypes on the sites and number of metastases in 166 patients with metastatic breast cancer from a single center were assessed; and the influence of molecular subtypes on the sites and number of metastases and OS in 15,322 metastatic cases among 329,770 patients with primary breast cancer from the Surveillance, Epidemiology and End Results database were assessed. Analysis of both datasets revealed that different molecular subtypes exhibited differences in the prevalence of different metastatic sites and number of metastases. A larger proportion of bone metastasis was observed in the hormone receptor (HR)+/human epidermal growth factor receptor 2 (HER2)+ subtype than in other subtypes, more lung metastasis was observed in the HR-/HER2+ subtype and more liver metastasis occurred in the HR+/HER2+ and HR-/HER2+ subtypes. Single-site metastasis was more common for the HR+/HER2- subtype than in other subtypes, while 2-3 sites of metastases were more common for the HR+/HER2+ subtype and ≥4 sites of metastases were more frequent in the HR-/HER2+ and HR-/HER2- subtypes. The mean OS of patients with primary breast cancer in the HR+/HER2- subtype group was the longest (78.5 months), while the HR-/HER2- group had the shortest mean OS (69.1 months). The mean OS of the metastatic HR+/HER2+ group was the longest (46.0 months), while the mean OS of the metastatic HR-/HER2- group was the shortest (18.5 months). In conclusion, the results of the present study suggested that different molecular subtypes of breast cancer have different metastatic behavior, as well as mean OS.Giant cell tumor of bone (GCTB) is an intermediate (locally aggressive) bone tumor with a recurrence rate of >30% following surgery. GCTB recurrence is ultimately due to the proliferation of neoplastic stromal (NS) cells. However, the precise mechanism underlying the regulation of NS cell proliferation remains unknown. p62 protein is a multifunctional adaptor protein that exerts a positive role in bone tumors and metabolic bone diseases. In the present study, the mRNA and protein expression levels of p62 were detected by reverse transcription-quantitative PCR and western blotting, respectively, in 8 paired fresh GCTB tumor tissues and adjacent normal cancellous bone tissues. The association between p62 expression level and patient prognosis was subsequently analyzed in 54 paraffin-embedded tumor specimens by immunohistochemistry assay. NS cells were isolated from GCTB primary cell culture, and the role of p62 was evaluated using in vitro cell proliferation, migration and invasion assays. The results revealed that p62 mRNA and protein were overexpressed in tumor tissues. High p62 expression levels were significantly associated with the recurrence of GCTB (P=0.001). The patients in the high p62 expression group had shorter 5-year recurrence-free survival rates compared with the patients in the low p62 expression group (P less then 0.001). Cox regression analysis identified p62 expression as an independent prognostic indicator of the recurrence-free survival of patients with GCTB (P less then 0.001). The in vitro experiments revealed that p62 downregulation inhibited NS cell proliferation, invasion and migration, and promoted apoptosis. In conclusion, it was found that p62 overexpression is associated with the recurrence of GCTB via the promotion of NS cell proliferation. Therefore, p62 could be a novel prognostic indicator, and a potential therapeutic target for GCTB.ZNF365 is a transcription factor that plays important roles in different types of cancer, such as colorectal cancer, breast cancer and hepatocellular carcinoma. ZNF365 can promote stalled replication fork recovery to prevent genomic instability, which is a notable feature of sporadic and hereditary types of cancers. However, the function of ZNF365 in the tumor progression of colorectal cancer (CRC) remains unclear. Thus, immunohistochemical staining was used to investigate the association between ZNF365 expression and the clinicopathological characteristics of patients with colorectal cancer. The results demonstrated that ZNF365 protein was strongly expressed in the nucleus and cytoplasm of normal colorectal mucosa. Furthermore ZNF365, which is methylated and downregulated in most cancer cell lines and tissues, was significantly associated with lymph node metastasis (P=0.015), depth of invasion (P=0.031) and histopathological grading (P=0.042). A positive correlation was observed between ZNF365 expression and phosphorylated (P)-p53 (Ser15) protein expression (r=0.18; P=0.038). Survival analysis indicated that patients with high ZNF365 expression had a higher survival rate than those with low ZNF365 expression (P=0.009), suggesting that ZNF365 may be an independent prognostic factor for survival in colorectal cancer (P=0.046). Taken together, the results of the present study demonstrated that ZNF365 was frequently inactivated by promoter methylation and independently predicted poor prognosis in patients with colorectal cancer by downregulating P-p53 (Ser15) expression.Breast cancer is a major health problem and accounted for 11.6% of all new cancer cases and 6.6% of all cancer deaths among women worldwide in 2018. However, its etiology has remained elusive. According to epidemiological studies, environmental factors are influencing the increase in the incidence of breast cancer risk. Components such as chemicals, including pesticides, are agents that produce deleterious effects on wildlife and humans. Among them, the organophosphorus pesticides, such as malathion, have largely been considered in this etiology. The epithelial-mesenchymal transition serves a key role in tumor progression and it is proposed that malathion is closely associated with the origin of this transition, among other causes. Moreover, proteins participating in this process are primordial in the transformation of a normal cell to a malignant tumor cell. The aim of the current study was to evaluate markers that indicated oncogenic properties. The results indicated greater expression levels of proteins associated with the epithelial-to-mesenchymal transition, including E-cadherin, Vimentin, Axl, and Slug in the rat mammary glands treated with malathion alone and combined with estrogen. Atropine was demonstrated to counteract the malathion effect as a muscarinic antagonist. The understanding of the use of markers in experimental models is crucial to identify different stages in the cancer process. The alteration of these markers may serve as a predicting factor that can be used to indicate whether a person has altered ducts or lobules in breast tissue within biopsies of individuals exposed to OPs or other environmental substances.Glioma is one of the most common types of tumor of the central nervous system. Due to the aggressiveness and invasiveness of high-level gliomas, the survival time of patients with these tumors is short, at ~15 months, even after combined treatment with surgery, radiotherapy and/or chemotherapy. Recently, a number of studies have demonstrated that long non-coding RNA (lncRNAs) serve crucial roles in the multistep development of human gliomas. Gliomas acquire numerous biological abilities during multistep development that collectively constitute the hallmarks of glioma. Thus, in this review, the roles of lncRNAs associated with glioma hallmarks and the current and future prospects for their development are summarized.5-Aminolevulinic acid-mediated photodynamic therapy (ALA-PDT) is a minimally invasive therapeutic modality used in the management of various cancers, but to a lesser extent for esophageal cancer (EC). The current study investigated the antitumor effects of ALA-PDT. Human EC cells were treated with ALA, after which ALA-induced fluorescence was examined under a fluorescence microscope. The cytotoxic effects of ALA-PDT were assessed using three types of LEDs (blue, green and red) in vitro and in vivo. Subcutaneous tumor model mice was constructed with KYSE150 cells. ALA-PDT was performed once a week for 4 weeks and tumor weights were measured. A popliteal lymph node (PLN) metastasis murine model was generated using KYSE150 cells. KYSE150 cells were inoculated into the left footpad of nude mice. ALA-PDT was performed on the footpad once a week for 4 weeks. PLNs were then removed 3 weeks after the last treatment. The lymph nodes were evaluated by hematoxylin and eosin staining. Red fluorescence of protoporphyrin IX (PpIX) was observed in all EC cell lines. ALA-PDT using LEDs exerted significant antitumor effects in vitro and in vivo. The antitumor effects of ALA-PDT with blue LED were the strongest, followed by green and red LEDs. The number of metastasized PLNs was significantly smaller in the ALA-PDT group (0%) than in the control group (37.5%). The present results indicated that ALA-PDT is effective for EC.Cancer is the leading cause of death worldwide. The absence of obvious symptoms and insufficiently sensitive biomarkers in early stages of carcinoma limits early diagnosis. Cancer therapy agents and targeted therapy have been used extensively against tissues or organs of specific cancers. However, the intrinsic and/or acquired resistance to the agents or targeted drugs as well as the serious toxic side effects of the drugs would limit their use. Therefore, identifying biomarkers involved in tumorigenesis and progression represents a challenge for cancer diagnosis and therapeutic strategy development. The eukaryotic translation factor 5A (eIF5A), originally identified as an initiation factor, was later shown to promote translation elongation of iterated proline sequences. There are two eIF5A isoforms (eIF5A1 and eIF5A2). eIF5A2 protein consists of 153 residues, and shares 84% amino acid identity with eIF5A1. However, the biological functions of these two isoforms may be significantly different. Recently, it was demonstrated that eIF5Ais widely involved in the pathogenesis of a number of diseases, including cancers. In particular, eIF5A plays an important role in regulating tumor growth, invasion, metastasis and tumor microenvironment. It was also shown to serve as a potential biomarker and target for the diagnosis and treatment of cancers. The present review briefly discusses the latest findings of eIF5A in the pathogenesis of certain malignant cancers and evolving clinical applications.Laryngeal squamous cell carcinoma (LSCC) is one of the most frequently diagnosed head and neck cancers worldwide. Increasing evidence suggests that microRNAs (miRNAs/miRs) regulate the progression of tumorigenesis and the malignant behaviors of cancer cells. The aim of this study was to investigate the function and underlying mechanism of miR-375-3p in LSCC. The expression of miR-375-3p in LSCC tissues and cells was detected using reverse transcription-quantitative PCR. The effects of miR-375-3p on the malignant phenotype of LSCC cells was determined using the Cell Counting Kit-8 assay and flow cytometry. The targets of miR-375-3p were predicted using the miRDB database and confirmed by the luciferase reporter assay. The results of the present study demonstrated that miR-375-3p was downregulated in LSCC tissues and cell lines. Furthermore, overexpression of miR-375-3p significantly suppressed the proliferation and cell cycle progression of LSCC cells. Overexpression of miR-375-3p also increased LSCC cell apoptosis. Mechanistical analysis indicated that miR-375-3p bound the 3'-untranslated region of the hepatocyte nuclear factor 1β (HNF1β) and decreased its expression in LSCC cells. Consistent with the role of HNF1β in glucose metabolism, overexpression of miR-375-3p significantly inhibited glucose consumption and lactate production in LSCC cells. Transfection with HNF1β notably reversed the inhibitory effect of miR-375-3p on the proliferation of LSCC cells. Collectively, these results indicate the tumor suppressive role of miR-375-3p in LSCC via HNF1β, suggesting that miR-375-3p may serve as a potential target in the treatment of LSCC.Zinc finger protein 281 (ZNF281) has been characterized as a tumor suppressive lncRNA in glioma. The present study aimed to analyze the functionality of ZNF281 in osteosarcoma (OS). It was demonstrated that ZNF281 was downregulated in OS tissue specimens and predicted the survival of patients with OS. In tissues from patients with OS, ZNF281 was negatively associated with rho-associated coiled-coil containing protein kinase 1 (ROCK1), but positively associated with miR-144. In the U2OS cell line, ZNF281 overexpression mediated the upregulation of miR-44 and downregulation of ROCK1. miR-144 overexpression led to the downregulation of ROCK1, but failed to affect ZNF281. Expression of ZNF281 and miR-144 resulted in decreased cell migration and invasion, while ROCK1 overexpression resulted in increased invasion and migration of OS cells. In addition, ROCK1 overexpression attenuated the effects of ZNF281 and miR-144 overexpression. Thus, ZNF281 may downregulate ROCK1 by upregulating miR-144 and inhibit cancer cell invasion and migration in OS.The present study aimed to verify the efficacy of the conditionally reprogrammed cell (CRC) culture method for the detection of circulating tumor cells (CTCs) in breast cancer. CTCs were isolated from the peripheral blood of patients with breast cancer, and culture of the collected CTCs was performed according to the conditional reprogramming protocol. Total RNA was extracted from cultured CTCs, and the hTERT and MAGE A1-6 genes were amplified using reverse transcription-PCR (RT-PCR). In addition, RNA extraction from another blood sample was performed and the expression of the two genes was analyzed by RT-PCR only. Following CRC culture, grown CTCs were observed in 7 samples (23.3%). The CTC detection rates by RT-PCR for the hTERT and MAGE A1-6 genes in CTCs grown using the CRC culture method were 26.7 and 10.0%, respectively. The positive expression rates for the hTERT and MAGE genes in CTCs assessed by RT-PCR only were 44.1 and 23.5%, respectively. When combining the positive expression rates of RT-PCR only and CRC culture for the hTERT and MAGE A1-6 genes, CTC detection rates increased to 53.3 and 23.3%, respectively. Additionally, when combining the positive expression rates of the two genes by either method, the CTC detection rate was the highest value observed. In conclusion, the present study revealed the potential of CRC culture in the detection of CTCs in breast cancer. Furthermore, a combination of CRC culture and RT-PCR for the hTERT and MAGE A1-6 genes is useful in enhancing the detection rate of CTCs in the blood.Breast lumpectomy is usually performed under general or local anesthesia. To the best of our knowledge, whether conscious sedation with intranasal dexmedetomidine and local anesthesia is an effective anesthetic technique has not been studied. Thus, the present study aimed to investigate the effectiveness of conscious sedation with intranasal dexmedetomidine combined with local anesthesia in breast lumpectomy, and to identify its optimal dose. A prospective randomized, double-blinded, placebo-controlled, single-center study was designed, and patients undergoing breast lumpectomies were recruited based on the inclusion and exclusion criteria. All patients were randomly allocated to four groups i) Local anesthesia with 0.9% intranasal saline (placebo); local anesthesia with ii) 1 µg.kg-1; iii) 1.5 µg.kg-1; or iv) 2 µg.kg-1 intranasal dexmedetomidine. The sedation status, pain relief, vital signs, adverse events, and satisfaction of patient and surgeon were recorded. Patients in the three dexmedetomidine groups wient satisfaction without adverse effects.Lung cancer is the leading cause of cancer-associated death worldwide. In recent years, the advancement of epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) targeted therapies has provided clinical benefits for lung cancer patients with EGFR mutations. The response to EGFR-TKI varies in patients with lung cancer, and resistance typically develops during the course of the treatment. Therefore, understanding biomarkers which can predict resistance to EGFR-TKI is important. Overexpression of GLI causes activation of the Hedgehog (Hh) signaling pathway and plays a critical role in oncogenesis in numerous types of cancer. In the present study, the role of GLI1 in erlotinib resistance was investigated. GLI1 mRNA and protein expression levels were determined using reverse transcription-quantitative PCR and immunohistochemistry (IHC) in lung cancer cell lines and tumor specimens, respectively. GLI1 mRNA expression levels were found to be positively correlated with the IC50 of erlotinib in 15 non-small cell lung cancer (NSCLC) cell lines. The downregulation of GLI1 using siRNA sensitized lung cancer cells to the erlotinib treatment, whereas the overexpression of GLI1 increased the survival of lung cancer cells in the presence of erlotinib, indicating that Hh/GLI activation may play a critical role in the development of TKI resistance in lung cancer. Combined treatment with erlotinib and a GLI1 inhibitor reduced the cell viability synergistically. A retrospective study of patients with NSCLC treated with erlotinib revealed that those with a high IHC score for GLI1 protein expression had a poorer prognosis. These results indicated that GLI1 is a key regulator for TKI sensitivity, and patients with lung cancer may benefit from the combined treatment of TKI and GLI1 inhibitor.Two-dimensional ultrasound (US) and color doppler flow imaging are associated with certain limitations in the preprocedural evaluation and design of the puncture path for biopsies of thoracic lesions, such as a poorly defined boundary between the tumor and the atelectatic lesions in central lung cancer with atelectasis. Contrast-enhanced ultrasound (CEUS) can be valuable in the preoperative evaluation of the biopsy site and in increasing the accuracy of the biopsy. The present study investigated the value of clinical application of CEUS in US-guided core needle biopsy (US-CNB) in improving the diagnostic accuracy in thoracic lesions. A total of 120 patients with first-stage thoracic lesions from the Affiliated Tumor Hospital of Guangxi Medical University who underwent US-CNB were recruited and randomnly assigned to a conventional US group (n=66) and a CEUS group (n=54). All patients underwent preoperative evaluation and US-guided puncture of thoracic lesions. The intergroup differences in sonographic features, biopsy duration, biopsy success rate and complications were assessed. The CEUS group had a higher rate of detection of necrotic tissue (40.7% vs. 16.7%; χ2=8.633; P=0.003) and change of initial puncture path (48.1%) compared with the US group. In central lung cancer with atelectasis, the ability to distinguish between tumor and atelectasis was higher in the CEUS group compared with the conventional US group (31.5 vs. 7.6%; χ2=11.336; P=0.001). In addition, the CEUS group had a higher puncture success (96.3 vs. 80.3%; χ2=6.946; P=0.008) and a lower complication rate (3.7% vs. 18.2%; χ2=6.041; P=0.014) compared with the US group. CEUS can identify necrotic areas and occult tumors within atelectatic lung tissue and can be used for guiding puncture biopsy of thoracic lesions to improve the diagnostic accuracy with greater comparative clinical utility than conventional US. Pre-biopsy CEUS is especially useful for patients undergoing repeated US-CNB and those with hypovascular lesions, atelectasis or necrosis.Hepatocellular carcinoma (HCC) is a malignant tumor with high incidence and high risk. Study of the role and mechanism of miRNAs are a hot spot of research providing new treatment ideas in malignant tumors. The effect of miR-642a on HCC progression and the underlying molecular mechanism were investigated. Expression of miR-642a and SEMA4C was measured by western blot analysis and RT-PCR. miR-642a expression was elevated while SEMA4C expression was attenuated in HCC tissues and cells. Results of luciferase reporter and western blot analyses show that miR-642a modulated SEMA4C expression by binding to its 3'UTR. Moreover, miR-642a negatively regulated SEMA4C expression. HCC cell migration and invasion was tested by Transwell assays. The findings revealed that the number of migrated and invaded cells were reduced by miR-642a mimic and raised by miR-642a inhibitor, indicating that miR-642a showed a suppression effect on HCC cell migration and invasion. Additionally, the migration and invasion of HCC cells were inhibited by SEMA4C siRNA, and SEMA4C reversed miR-642a effect on HCC migration and invasion. Furthermore, p38 MAPK signaling pathway was proven to be inhibited by miR-642a mimic, whereas facilitated by miR-642a inhibitor and SEMA4C siRNA could overturn the promotion effect of miR-642a inhibitor. Briefly, miR-642a targeted SEMA4C to repress HCC cell migration and invasion through p38 MAPK signaling pathway providing a new strategy for treatment of HCC patients.Melanoma is a common type of cutaneous tumor, but current drug treatments do not satisfy clinical practice requirements. At present, mitochondrial uncoupling is an effective antitumor treatment. Triclosan, a common antimicrobial, also acts as a mitochondrial uncoupler. The aims of the present study were to investigate the effects of triclosan on melanoma cells and the underlying mechanisms. Mitochondrial membrane potential (MMP), mitochondrial morphology, mitochondrial reactive oxygen species (mito-ROS), intracellular superoxide anion and [Ca2+]i were measured using confocal microscopy. It was found that triclosan application was associated with decreased A375 cell viability in a dose- and time-dependent manner and these effects may have cell specificity. Furthermore, triclosan induced MMP depolarization, ATP content decrease, mito-ROS and [Ca2+]i level increases, excessive mitochondrial fission, AMP-activated protein kinase (AMPK) activation and STAT3 inhibition. Moreover, these aforementioned effects were reversed by acetylcysteine treatment. Triclosan acute treatment also induced mitochondrial swelling, which was reversed after AMPK-knockdown associated with [Ca2+]i overload. Cell death was caused by STAT3 inhibition but not AMPK activation. Moreover, triclosan induced autophagy via the ROS/AMPK/p62/microtubule-associated protein 1A/1B-light chain 3 (LC3) signaling pathway, which may serve a role in feedback protection. Collectively, the present results suggested that triclosan increased mito-ROS production in melanoma cells, following induced cell death via the STAT3/Bcl-2 pathway and autophagy via the AMPK/p62/LC3 pathway.Tumor necrosis factor-related apoptosis inducing ligand (TRAIL)-mediated apoptosis is a safe method for the treatment of various types of cancer. However, TRAIL therapy is less effective in certain types of cancer, including cervical cancer. To address this problem, a combinatorial approach was employed to sensitize cervical cancer at low dosages. YM155, a survivin inhibitor, was used at low dosages along with TRAIL to induce apoptosis in HeLa cells. The effects of the individual treatment with TRAIL and YM155 on apoptosis were assessed by propidium iodide assay. In addition, to validate the DNA damage exhibited by the combination treatment, the phosphorylation status of γH2A histone family member X was investigated by immunofluorescence and western blot analysis. TRAIL or YM155 alone had no significant effect on DNA damage and apoptosis. However, the TRAIL/YM155 combination triggered a synergistic pro-apoptotic stimulus in HeLa cells. The mRNA and protein levels of CASP8- and FADD-like apoptosis regulator (cFLIP), death receptor 5 (DR5) and survivin were monitored using RT-PCR and western blot analysis, respectively. This combinatorial approach downregulated both mRNA and protein expression levels of cFLIP and survivin. Further experimental results suggested that the combination treatment significantly reduced cell viability, invasion and migration of HeLa cells. Overall, the present findings indicated that the low dosage of YM155 sensitized HeLa cells to TRAIL-induced apoptosis via a mechanism involving downregulation of cFLIP and survivin. The results indicated the importance of combination drug treatment and reveal an effective therapeutic alternative for TRAIL therapy in human cervical cancer.Hepatocellular carcinoma (HCC) remains a challenge in the medical field due to its high malignancy and mortality rates particularly for HCC, which has developed multidrug resistance. Therefore, the identification of efficient chemotherapeutic drugs for multidrug resistant HCC has become an urgent issue. Natural products have always been of significance in drug discovery. In the present study, a cell-based method was used to screen a natural compound library, which consisted of 78 compounds, and the doxorubicin-resistant cancer cell line, HepG2/ADM, as screening tools. The findings of the present study led to the shortlisting of one of the compounds, digitoxin, which displayed an inhibitory effect on HepG2/ADM cells, with 50% inhibitory concentration values of 132.65±3.83, 52.29±6.26, and 9.13±3.67 nM for 24, 48, and 72 h, respectively. Immunofluorescence, western blotting and cell cycle analyses revealed that digitoxin induced G2/M cell cycle arrest via the serine/threonine-protein kinase ATR (ATR)-serine/threonine-protein kinase Chk2 (CHK2)-M-phase inducer phosphatase 3 (CDC25C) signaling pathway in HepG2/ADM cells, which may have resulted from a DNA double-stranded break. Digitoxin also induced mitochondrial apoptosis, which was characterized by changes in the interaction between Bcl-2 and Bax, the release of cytochrome c, as well as the activation of the caspase-3 and -9. To the best of our knowledge, the present study is the first report that digitoxin displays an anti-HCC effect on HepG2/ADM cells through G2/M cell cycle arrest, which was mediated by the ATR-CHK2-CDC25C signaling pathway and mitochondrial apoptosis. Therefore, digitoxin could be a promising chemotherapeutic agent for the treatment of patients with HCC.Reliable biomarkers for the prognosis of hepatocellular carcinoma (HCC) are rare, and novel biomarkers are required for the appropriate management of HCC. 5'-Nucleotidase domain containing 2 (NT5DC2) acts as an oncogene in various tumors, but its functions as a biomarker have not been confirmed. Therefore, the present study aimed to resolve these functions by analyzing the prognostic value of NT5DC2 in patients with HCC. A tissue microarray (TMA) was prepared and NT5DC2 expression was measured via IHC staining in TMA dots. The liver cancer (LIHC) cohort in The Cancer Genome Atlas (TCGA) was enrolled as a secondary cohort. Kaplan-Meier survival analyses and Cox regression models were used for assessment of the prognostic value of NT5DC2. Gene set enrichment analysis (GSEA) was performed in TCGA LIHC cohort. A total of 134 patients with HCC were retrospectively enrolled in the Peking Union Medical College Hospital cohort and clinical data were collected. A total of 359 patients with HCC in TCGA were enrolled as TCGA cohort. NT5DC2 was used as an indicator of overall survival (OS) and relapse-free survival (RFS) in multiple cohorts. In the multivariate Cox regression model, NT5DC2 upregulation was an independent prognostic factor of OS in both cohorts. GSEA indicated the enrichment of a series of survival- and metastasis-related gene-sets, such as LEE_LIVER_CANCER_SURVIVAL_UP and LIAO_METASTASIS. Collectively, it was suggested that NT5DC2 upregulation was associated with poor OS and RFS in HCC, and was a potential predictive marker for HCC stratification.Laryngeal cancer is a common head and neck cancer that effects the quality of life of those affected. Early diagnosis and treatment are vital to minimize the harmful effects of laryngeal cancer, which can improve the survival rate of patients following surgery and retain the voice function of the larynx. The purpose of the present study was to explore the molecular mechanism of the development of laryngeal cancer and to determine the biomarker for the diagnosis and treatment of laryngeal cancer. Reverse transcription-quantitative PCR (RT-qPCR) and The Cancer Genome Atlas database analysis were used to confirm high expression of TMEM158 in laryngeal cancer. The effects of TMEM158 and miR-548ac was investigated through in vitro and in vivo assays (MTT assay, colony-formation assay, flow cytometry assay, western blotting and tumor xenograft assay). Luciferase reporter assay, western blotting and RTq-PCR were used to confirm that miR-548 directly targeted the 3'-untranslated region of TMEM158 and inhibited TMEM158 expression. Taken together, the present results suggest that miR-548ac functions as a crucial cancer suppressor in laryngeal cancer, which induces apoptosis in laryngeal cancer cells by suppressing TMEM158. Thus, miR-548ac may be a potential target for the treatment of laryngeal cancer.MicroRNAs (miRs) are associated with cancer metastasis. Aberrant expression levels of members of the miR-30 family have been observed in non-small-cell lung cancer (NSCLC). However, the effects of miR-30 family members on the epithelial-to-mesenchymal transition (EMT) of NSCLC cells and the underlying molecular mechanisms have not yet been fully elucidated. The present study investigated the effects of miR-30 family members on EMT, migration and invasion of NSCLC cells and found that overexpression of these miRs inhibited EMT via decreasing the expression levels of N-cadherin, β-catenin and SNAI1, along with weakened migration and invasion abilities. Then, XB130 was identified as a downstream target of the miR-30 family members. XB130-knockdown also inhibited EMT of NSCLC cells, whereas ectopic overexpression of XB130 partly rescued the suppressive effects of miR-30c and miR-30d on EMT. In conclusion, miR-30 family members inhibited EMT of NSCLC cells, partially via suppressing XB130 expression levels.Micheliolide (MCL), a sesquiterpene lactone isolated from Michelia compressa and Michelia champaca, has been used previously to inhibit the NF-κB signaling pathway. MCL has exerted various therapeutic effects in numerous types of disease, such as inflammatory and cancer. However, to the best of our knowledge, its underlying anticancer mechanism remains to be understood. The present study aimed to investigate the effects of MCL on human glioma U251MG cells and to determine the potential anticancer mechanism of action of MCL. From Cell Counting Kit-8, colony formation assay, apoptosis assay and Confocal immunofluorescence imaging analysis, the results revealed that MCL significantly inhibited cell viability in vitro and induced cell apoptosis via activation of the cytochrome c/caspase-dependent apoptotic pathway. In addition, MCL also suppressed cell invasion and metastasis via the wound healing and Transwell invasion assays. Furthermore, western blot and reverse transcription PCR analyses demonstrated that MCL significantly downregulated cyclooxygenase-2 (COX-2) expression levels, which may have partially occurred through the inactivation of the NF-κB signaling pathway. In conclusion, the results of the present study indicated that MCL may inhibit glioma carcinoma growth by downregulating the NF-κB/COX-2 signaling pathway, which suggested that MCL may be a novel and alternative antitumor agent for the treatment of human glioma carcinoma.Alkylglycerone phosphate synthase (AGPS) is a key enzyme for ether ester synthesis and acts as an oncogene in malignant tumors. The present study aimed to investigate the effect of AGPS silencing on the expression levels of long non-coding RNAs (lncRNAs) and the co-expression with mRNAs in glioma U251 cells using microarray analysis. Furthermore, the underlying biological functions of crucial lncRNAs identified were investigated. It was discovered that in vitro U251 cell proliferation was suppressed following the genetic silencing of AGPS. Differentially expressed lncRNAs and mRNAs in U251 cells were sequenced following AGPS silencing. The results from the Gene Ontology analysis identified that the co-expressed mRNAs were mainly involved in biological processes, such as 'cellular response to hypoxia', 'extracellular matrix organization' and 'PERK-mediated unfolded protein response'. In addition, Kyoto Encyclopedia of Genes and Genomes signaling pathway enrichment analysis revealed that the co-expressed mRNAs were the most enriched in the 'AGE/RAGE signaling pathway in diabetic conditions'. Additionally, the PI3K/Akt and epidermal growth factor receptor signaling pathways serve important roles in tumor processes, for example carcinogenesis and angiogenesis. Furthermore, it was identified that the lncRNA AK093732 served a vital role in the regulatory network and the core pathway in this network regulated by this lncRNA was discovered to be the 'Cytokine-cytokine receptor interaction'. In conclusion, the findings of the present study suggested that AGPS may affect cell proliferation and the degree of malignancy. In addition, the identified lncRNAs and their co-expressed mRNAs screened using microarrays may have significant biological effects in the occurrence, development and metastasis of glioma, and thus may be novel markers of glioma.Laryngeal carcinoma is a common head and neck malignancy, however, the molecular mechanism of the disease has not yet been elucidated. The present study aimed to investigate the role of IGF1R antisense imprinted non-protein coding RNA (IRAIN) long non-coding (lnc)RNA in laryngeal carcinoma. In total, specimens of healthy pharynx tissue from 6 healthy individuals, carcinoma tissue and paracancerous tissue from 37 patients with laryngeal carcinoma were used in this study. The single nucleotide polymorphism (SNP) rs8034564 was used to distinguish the two parental alleles of IRAIN. DNA and RNA were extracted from tissue specimens and the IRAIN allelic gene was sequenced. Reverse transcription-quantitative PCR was used to determine the expression levels of IRAIN and Insulin-like growth factor 1 receptor (IGF1R) in laryngeal carcinoma and paracancerous tissue. Bisulfite genomic sequencing was used to determine IRAIN promoter DNA methylation status in laryngeal carcinoma tissue. The expression of IRAIN was di-alleliof IRAIN allelic expression imbalance and aberrant allele-switch may serve as an early diagnostic marker of laryngeal carcinoma.Osteosarcoma (OS) occurs in both children and adolescents and leads to a poor prognosis. 2-methoxyestradiol (2-ME) has a strong antitumor effect and is effective against numerous types of tumor. However, 2-ME has a low level of antitumor effects in OS. The present study investigated the effects of 2-ME on the proliferation and apoptosis of human MG63 OS cells. The potential biological mechanisms by which 2-ME exerts its biological effects were also investigated in the present study. The results of the present study demonstrated that 2-ME inhibited the proliferation of OS cells in a time- and dose-dependent manner, induced G2/M phase cell cycle arrest and early apoptosis. The expression levels of vascular endothelial growth factor (VEGF), Bcl-2 and caspase-3 were measured via western blotting and reverse transcription-quantitative PCR. As the concentration of 2-ME increased, the RNA and protein expression levels of VEGF and Bcl-2 decreased gradually, whereas the expression of caspase-3 increased gradually. In addition, tumor growth in nude mice was suppressed by 2-ME with no toxic side effects observed in the liver or kidney. Immunohistochemistry demonstrated that the expression levels of Bcl-2 and VEGF were significantly lower, and those of caspase-3 were significantly higher in test mice compared with the control group. TUNEL staining of xenograft tumors revealed that with increased 2-ME concentration, the number of apoptotic cells also gradually increased. Thus, 2-ME effectively inhibited the proliferation and induced apoptosis of MG63 OS cells in vitro and in vivo with no obvious side effects. The mechanism of the anticancer effect of 2-ME may be associated with the actions of Bcl-2, VEGF and caspase-3.Long non-coding RNAs (lncRNAs) can act as competing endogenous RNAs (ceRNAs), interacting with microRNAs (miRNAs) and playing an important role in tumor progression. However, the role of lncRNA-mediated ceRNAs in glioma remains largely unknown. The present study aimed to identify novel lncRNAs and their associated function in glioma. RNA sequencing and corresponding clinical data from patients with glioma were obtained from The Cancer Genome Atlas. A total of 598 glioma tissues and 5 normal brain tissues were analyzed in the present study. The differentially expressed (DE) lncRNAs, mRNAs and miRNAs were identified using R packages and were used to construct a ceRNA network. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses were performed to investigate the biological functions of the DEmRNAs. Kaplan-Meier curve analysis was performed to investigate the association between DElncRNA expression and patient outcome. A total of 752 DElncRNAs, 2,079 DEmRNAs and 113 DEmiRNAs were identified between glioma and normal tissues. A lncRNA-miRNA-mRNA ceRNA network consisting of 61 lncRNAs, 12 miRNAs and 92 mRNAs was constructed. Survival analysis indicated that 36 DElncRNAs, 72 DEmRNAs and 3 DEmiRNAs were associated with overall survival in patients with glioma. The present study identified novel lncRNAs associated with survival prognosis and may facilitate further investigation of lncRNA-mediated ceRNA regulatory mechanisms in glioma.