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Gastric cancer is one of the most severe cancers, while the relationship between Helicobacter pylori (H. pylori) and gastric cancer are still in dispute, and little work has been done to explore the microbial diversity between H. pylori positive patients and negative patients. In the present work, a total of 43 gastric cancer patients and 10 healthy 53 participants were enrolled to compare the microbial differences in community structure in gastrointestinal tract between H. pylori positive patients and negative patients with gastric cancer. Our results indicated that the abundance and diversity of gastrointestinal microbiota was slight lower in gastric cancer patients than that in healthy participants especially in intestine, while the abundance of some potential pathogens, e.g. Streptococcus, Lactobacillus, Akkermansia and Halomones were higher in H. pylori positive patients than H. pylori negative patients. Therefore, our work suggests the various microbial diversity between H. pylori positive patients and H. pylori negative patients with gastric cancer, which contribute to deepen the understanding of the role of H. pylori in gastric carcinogenesis and progression.Background Multidrug resistance gene 1 (MDR-1) encodes for P-glycoprotein (P-gp) recognized for removing cytostatic drugs from tumor cells. MDR1 gene polymorphisms change function of P-gp. In this study, we are interested in investigating whether MDR1 C1236T single nucleotide polymorphisms (SNPs) affect the susceptibility and treatment-related toxicities in B-cell non-Hodgkin lymphoma (B-NHL) in the population of eastern China. Materials and methods A group of 107 B-NHL patients and 150 healthy donors, unrelated ethnic Han Chinese and residents of eastern China, were included in this study. The MDR1 C1236T polymorphisms were determined using polymerase chain reaction-allele specific primers after extraction of genomic DNA. Analyses were performed using SPSS and Arlequin software. Results MDR1 C1236T polymorphisms were not significantly related to the risk and treatment-related toxicities of B-NHL. A significant association between extranodal sites and C1236T allele was observed (C vs T P=0.01). Conclusion Our findings could expand our understanding of MDR1 in B-NHL and provide references for further research in multidrug resistance.Background Wilms tumor gene on X chromosome (WTX) is an X-linked tumor suppressor gene in Wilms tumor; however, however, the molecular mechanism of WTX in the occurrence and development of HCC has not been reported. Methods The expression of miR-454-3p and WTX wre analyzed in 32 matched human HCC and normal tissue samples. The molecular mechanisms of miR-454-3p/WTX/TGFβ signaling in cell proliferation, migration, invasion and autophagy were investigated in vitro and in vivo. Results WTX expression was downregulated in HCC tissues; lower WTX levels were associated with poor HCC patient outcomes. WTX loss triggers the activation of TGF-β signaling, which promotes HCC cells proliferation, migration, invasion and autophagy. Further mechanistic study showed that the aberrant upregulation of miR-454-3p was identified as the reason of WTX loss in HCC. Conclusions WTX is a tumor suppressor gene in HCC, miR-454-3p/WTX/TGFβ signaling will provide a new direction for the diagnosis and treatment of HCC.Purpose This study aimed to explore a predictive risk-stratification model combing clinical characteristics and lipid profiles in multiple myeloma (MM) patients. Methods The data of 275 patients in Sun Yat-Sen University Cancer Center were retrospectively analyzed and randomly divided into the training (n = 138) and validation (n=137) cohorts. Triglyceride (TG), low-density lipoprotein (LDL), high-density lipoprotein (HDL), lactate dehydrogenase (LDH), Apolipoprotein B (Apo B) and Apo B/Apolipoprotein A1 (Apo A1) ratio were the prognostic factors identified through univariate and multivariate Cox analysis. Results A 6-prognostic factor model was constructed based on Lasso regression. Patients were divided into low- and high-risk groups and the former group showed longer overall survival (OS) time (p less then 0.05). The area under the curve (AUC) of the risk score model for 5-and 10-year OS were 0.756 [95% CI 0.661-0.850] and 0.940 [95% CI 0.883-0.997], which exhibited better accuracy than International Staging System (ISS) and Durie and Salmon (DS) stage. Conclusion This study aims to combine the lipid metabolism profile with the clinical characteristics of MM patients to generate a prognostic model. The nomogram integrating ISS stage and risk score increased the prediction accuracy. This model can monitor lipid profile as a simple and effective method, which has certain clinical significance for improving the accuracy of the prognosis and exploring potential therapeutic targets.Background Logarithmic ratio of positive lymph nodes (LODDS), number of positive lymph nodes (NPLN), and number of lymph nodes to positive lymph nodes (pLNR) are three lymph node classifications; however, their function in prognosis is unclear. Purpose To establish and validate an optimal nomogram according to the comparison among the 7th TNM stage of American Joint Committee on Cancer (AJCC) and the three lymph node classifications. Methods A total of 881 patients from the Surveillance, Epidemiology and End Result (SEER database) with T1-4N1-3M0 in laryngeal squamous cell carcinoma from 2000 to 2018 were involved. The enrolled patients were allocated randomly into a training cohort and a validation cohort. Univariate cox regression analysis and multivariable cox regression analysis were applied to explore the predictors. The Akaike Information Criterion (AIC) and Harrell's concordance index (C-index) were to measure the predictive value and the accuracy of the prognostic models. Moreover, integrated discrimination improvement (IDI) and net reclassification index (NRI) were also used to assess the predictive abilities to models. According to the optimal model, nomograms were established and compared with 7th TNM stage of AJCC via the decision curve analysis. Results NPLN, LODDS, and pLNR were three predictors for the overall and cancer-specific survival in the larynx squamous cell carcinoma. According to the AIC, C-index, IDI, and NRI, the model of NPLN combined with LODDS was assumed as the optimal prognostic model. Lorlatinib Moreover, the decision curve analysis suggested that the nomogram demonstrated a better predictive performance, compared with the 7th AJCC TNM stage. Conclusion The proposed nomograms we constructed for larynx squamous cell carcinoma has potential in the prediction of patients after surgery.To investigate the important roles of the cancer-promoting long non-coding RNAs (lncRNAs) in cervical cancer, the up-regulated lncRNAs and prognostic analysis were identified through Lnc2Cancer and Lncar. LncRNA-regulated miRNA and miRNA-target mRNA were analyzed based on starBase v2.0 and miTarbase to predict the lncRNA-miRNA-mRNA ceRNA network. Based on the above findings, the abnormally expressed histocompatibility leukocyte antigen complex P5 (HCP5) was identified in 31 cervical cancer patients through RT-qPCR. The stable cell lines were constructed to explore the effect of HCP5 on the promotion of cervical cancer and the regulatory role on the expression of miR-216a-5p and CDC42. Cell Counting Kit-8 (CCK8) assay, cell clone formation, and transwell assay were used to examine proliferation and migration ability of cervical cancer cells. The results displayed that the overexpression of HCP5 promoted cervical cancer cell proliferation and migration in vitro, and the elevated HCP5 can also promote tumor growth in vivo. Besides, RT-qPCR and western blot assay revealed that elevated HCP5 suppressed miR-216a-5p expression and then up-regulated the expression of CDC42. In contrast, knocking down HCP5 resulted in increased expression of miR-216a-5p and then downregulated the expression of CDC42. Rescue experiments also demonstrated that miR-216a-5p could in part intercept in promotion impact caused by HCP5 on cervical cancer cells. Above all, HCP5, as an oncogene, can promote proliferation and migration ability of cervical cancer via the regulation of the miR-216a-5p/CDC42 axis.The eukaryotic chaperonin family is vital for cell survival. The dysregulation of chaperonin-containing TCP-1 subunit 3 (CCT3) is implicated in several types of malignant tumors' development. However, its functional role in melanoma remains unknown. Here we elucidate the functional contribution to CCT3 to melanoma progression. The results indicated that CCT3 highly expressed in melanoma tissues, and CCT3 overexpression is correlated with clinical stage in melanoma patients. Knockdown of CCT3 by shRNA in melanoma cells inhibited cell proliferation and cell cycle progression and induced cell apoptosis in vitro. In vivo, tumor growth in the nude mice was significantly inhibited after CCT3 silencing. Importantly, the gene array analysis showed that CCT3 depletions inhibited cyclins and cell cycle regulation signaling and further evaluation demonstrated that CDK1 expression was significantly decreased after CCT3 knockdown. Additionally, Functional rescues experiments also indicated that decreased cell proliferation due to CCT3 silencing was rescued by CDK1 overexpression. Overall, our findings suggest that CCT3 depletions prohibited melanoma progression by downregulating CDK1 expression and is a potential therapeutic target for melanoma.Colorectal cancer (CRC) is a highly malignant cancer with poor prognosis. MiR-211-5p has been widely studied as an antioncogene; however, its function and mechanism in CRC are still unknown. This study aimed to investigate the expression patterns and biological implications of miR-211-5p in CRC. This study used quantitative real-time polymerase chain reaction to evaluate miR-211-5p expression in CRC cells and tissues. MiR-211-5p mimics were constructed to overexpress miR-211-5p in Lovo and SW480 cells. Tumor bioactivities of CRC, including cell proliferation, migration, invasion, and colony formation, were evaluated. The dual-luciferase assay was used to confirm the targeted relationship between miR-211-5p expression and secreted protein acidic and rich in cysteine (SPARC). In addition, Western blot analysis and immunohistochemical staining were used to measure SPARC, platelet-derived growth factor (PDGF), transforming growth factor β (TGF-β), and vascular endothelial growth factor (VEGF) expression levels. This study showed downregulated miR-211-5p expression in CRC cells and tissues, and this downregulation correlated with CRC progression. Meanwhile, miR-211-5p restrained CRC cell proliferation, colony formation, migration, and invasion. Mechanistically, SPARC-related growth factor pathways, including VEGF, PDGF, and TGF-β pathways, were upregulated in CRC tissues. Furthermore, SPARC acted as the target gene for miR-211-5p. Finally, SPARC overexpression suppressed the inhibitory effect of miR-211-5p on CRC cell progression. MiR-211-5p suppressed the invasion, migration, proliferation, and progression of CRC cells through sponging SPARC-related growth factor pathways.Intrahepatic cholangiocarcinoma (ICC) is the most common malignant bile duct tumor in the liver and the second most common primary liver cancer with increasing morbidity and poor prognosis. Metabolic aberration plays key roles in cancer progression. As a key metabolic intermediate, acetyl-CoA accumulation shows close association with cancer metastasis. However, the role of acetyl-CoA metabolic aberration in ICC is still undetermined. Here, by investigating tissue samples from ICC patients and ICC cell lines, we found that acyl-CoA thioesterase 12 (ACOT12) expression is significantly down-regulated in ICC tissues, and is associated with poor prognosis of ICC. In vitro and in vivo studies demonstrated that ACOT12 suppressed ICC cells metastasis. Further mechanistic studies revealed that down-regulation of ACOT12 promoted ICC metastasis by inducing Slug expression and epithelial-mesenchymal transition (EMT). Our findings link ACOT12-regulated-acetyl-coA metabolic aberration with ICC metastasis and imply that ACOT12 could be a prognostic marker and a potential therapeutic target for ICC metastasis.