Timmonscormier0836

The dysregulation of lncRNA TMPO antisense RNA 1 (TMPO-AS1) has been detected in various malignant tumors. However, the role of lncRNA TMPO-AS1 remains unclear in pancreatic carcinoma. The present study aimed to elucidate the functional mechanism of TMPO-AS1 in pancreatic carcinoma. In the present study, RT-qPCR, western blotting, MTT, Transwell, luciferase reporter and xenograft assays were used to investigate the role of lncRNA TMPO-AS1 in pancreatic carcinoma. Upregulation of lncRNA TMPO-AS1 was revealed in pancreatic carcinoma tissues and cells. Furthermore, knockdown of TMPO-AS1 restrained cell proliferation and motility in pancreatic carcinoma. In addition, microRNA (miR)-383-5p acted as a 'sponge' for lncRNA TMPO-AS1. The expression levels of lncRNA TMPO-AS1 and miR-383-5p were mutually inhibited in pancreatic carcinoma. Moreover, miR-383-5p was revealed to directly target SRY-related high-mobility group box 11 (SOX11). Notably, SOX11 could promote the occurrence of pancreatic carcinoma by interacting with the lncRNA TMPO-AS1/miR-383-5p axis. In conclusion, upregulation of lncRNA TMPO-AS1 promoted tumor growth, cell migration and invasion in pancreatic carcinoma by downregulating miR-383-5p and upregulating SOX11.The undetectable onset of glioma and the difficulty of surgery lead to a poor prognosis. Appropriate biomarkers for diagnosis and treatment need to be identified. Interleukin-1 receptor-associated kinase 4 (IRAK4) is involved in the initiation and progression of cancer. However, up until now, no report has revealed the relationship between IRAK4 and glioma. The present study aimed to examine the expression of IRAK4 in glioma, and to determine if there was a relationship between IRAK4 expression and clinical outcomes or survival prognosis. Thousands of glioma tissue samples and corresponding clinical information were obtained from various databases. Then a series of bioinformatics methods were used to reveal the role of IRAK4 in glioma. Finally, reverse transcription-quantitative PCR technology was used to verify the bioinformatics results. The study found that the expression of IRAK4 was significantly increased in glioma compared with the control brain tissue samples, and IRAK4, as an independent prognostic factor, shortened the overall survival time of patients with glioma. Gene Set Enrichment Analysis showed that IRAK4 promoted the activation of cell signalling pathways, such as NOD-like and Toll-like receptor signalling pathways. Co-expression analysis showed that the expression of IRAK4 was correlated with CMTM6, MOB1A and other genes. The present study demonstrated the role of IRAK4 as an oncogene in the pathological process of glioma for the first time, and highlights the potential of IRAK4 as a biomarker for prognostic evaluation and treatment of glioma.Reports on the expression of interleukin (IL)-10 in breast cancer are rare. The present study investigated the correlation between IL-18 and -10 in breast cancer, and assessed their clinical significance. Breast cancer (n=104) and breast fibroadenoma (n=31) tissues that were surgically removed and pathologically confirmed at Jinan Central Hospital Affiliated to Shandong University (Jinan, China) between November 2016 and January 2019 were collected. The expression of IL-18 and -10 was observed via immunohistochemistry. Breast cancer tissues were positive for IL-18 expression, which was primarily located in the cell membrane and cytoplasm. A significant difference in IL-18 expression was observed between breast cancer and fibroadenoma tissues (75.0 vs. 19.4%; P less then 0.001). (L)-Dehydroascorbic mw IL-10 was expressed in breast cancer tissues and primarily located in the cytoplasm. Breast cancer tissues showed a significantly higher level of IL-10 expression compared with breast fibroadenoma tissues (78.8 vs. 22.6%; P less then 0.001). The regions of positive IL-18 and -10 expression were consistent. Tissues with positive expression of IL-18 and/or -10 had a significantly higher rate of lymph node metastasis than those with negative expression (IL-18 67.9 vs. 42.3%; P=0.035; and IL-10 67.1 vs. 40.9%; P=0.047). In conclusion, IL-18 is highly expressed in breast cancer and correlates positively with IL-10. Both IL-18 and -10 may correlate positively with lymph node metastasis in breast cancer.Glioma is the most common primary brain tumor and glioblastoma multiforme (GBM) is the most malignant brain glioma with the worst prognosis. T cell immune regulator 1 (TCIRG1) constitutes the V0a3 subunit of vacuolar ATPase (V-ATPase), and the function of V-ATPase in malignant tumors, such as breast cancer, melanoma and hepatocellular carcinoma, has been reported. However, the effect of the TCIRG1 subunit on GBM remains to be fully elucidated. mRNA levels of TCIRG1 in different cancer types and the corresponding normal tissues were extracted from the Oncomine and Tumor Immune Estimation Resource (TIMER) databases. The Gene Expression Omnibus (access number GSE16011), the Chinese Glioma Genome Atlas and The Cancer Genome Atlas were used to investigate the mRNA level of TCIRG1 in glioma. Protein level validation in glioma was performed using western blotting. The Database for Annotation, Visualization and Integrated Discovery was used to analyze Gene Ontology (GO) categories for genes correlated with TCIRG1 in therefore speculated that TCIRG1 is associated with glioma malignancy and may be a marker of unfavorable prognosis in patients with GBM, and it could be regarded as a prognostic biomarker and an indicator of immune infiltration in GBM.Dipyridamole, a traditional anti-platelet drug, has been reported to inhibit the proliferation of cancer cells. The present study aimed to investigate the possibility of dipyridamole as an adjuvant of chemotherapy by enhancing the cytotoxicity of an anti-cancer drug. The cytotoxicity of colorectal cancer cells (HCT-8), CD133+/CD44+ stem-like subpopulation of HCT-8 cells and lymphoma cells (U937) to dipyridamole and/or doxorubicin was evaluated using MTT proliferation and colony forming assays. The expression levels of phosphorylated cAMP-regulatory element-binding protein (pCREB) and poly(ADP-ribose) polymerase-1 (PARP-1) in cells were analyzed via western blotting and immunofluorescence. The present study reported controversial data regarding the anti-cancer effect of dipyridamole. Dipyridamole increased, rather than inhibited, the proliferation of HCT-8 and U937 cells in a dose-dependent manner. Furthermore, it was found that dipyridamole significantly increased the expression levels of pCREB and PARP-1. However, the combined usage of dipyridamole significantly enhanced the cytotoxicity of doxorubicin to HCT-8 cells at particular doses. Based on the current findings, dipyridamole likely induces the phosphorylation of CREB to promote the proliferation of cancer cells, but may enhance the cytotoxicity of anti-cancer drugs at particular doses.Colorectal cancer (CRC) is one of the most common solid tumors worldwide and has an extremely poor prognosis. MicroRNA-429 (miR-429) has been reported to participate in the progression of CRC. However, the pathological mechanisms require further investigation. The aim of the present study was to investigate the association between miR-429 and high mobility group box 3 (HMGB3) in CRC and the associated mechanism. The mRNA expression levels of miR-429 and HMGB3 in 65 paired CRC and adjacent tissues were examined by reverse transcription-quantitative PCR. Furthermore, a dual-luciferase reporter assay was performed to identify the association between miR-429 and HMGB3. Finally, the effects of miR-429 and HMGB3 on the proliferation and apoptosis of CRC cells were detected. As a result, it was identified that miR-429 expression was downregulated and HMGB3 expression was upregulated in CRC tissues compared with in adjacent non-cancer tissues, and the expression levels of miR-429 were negatively associated with those of HMGB3. Notably, HMGB3 was demonstrated to be a direct target of miR-429 by dual-luciferase reporter assay. Furthermore, transfection with a miR-429 mimic significantly inhibited HMGB3 expression and led to decreased proliferation and increased apoptosis of CRC cells. On the other hand, transient overexpression of HMGB3 partially inhibited the antitumor effects of miR-429. To the best of our knowledge, the present study demonstrated for the first time that miR-429 regulated the proliferation and apoptosis of CRC cells via HMGB3, suggesting a specific tumor suppressive function of the miR-429/HMGB3 signaling pathway in CRC.The determination of biomarkers in the blood specific for lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) is crucial for the selection of effective treatment strategies and the prediction of prognosis. The purpose of the present study was to analyze the differentially expressed genes (DEGs) in LUSC and LUAD from The Cancer Genome Atlas (TCGA) database. In order to identify the potential biomarkers for non-small cell lung cancer (NSCLC) for clinical diagnosis, bioinformatics was used to analyze the DEGs of two subtypes of NSCLC, LUAD and LUSC. Exosomes were isolated from the serum of patients with LUAD or LUSC and identified using transmission electron microscopy, nanoparticle tracking analysis and western blot analysis. A total of four differential exosomal mRNAs were selected for validation with serum samples from 70 patients with NSCLC via reverse transcription-quantitative polymerase chain reaction. Receiver operating characteristic curves were established to evaluate the clinical diagnoeir differential diagnosis and treatment.Colorectal carcinoma (CRC) is one of the most common malignant tumors. The present study aimed to investigate a non-invasive molecular marker that can evaluate the diagnosis and potential molecular mechanism of CRC. Microarray assays and reverse transcription-quantitative PCR analysis demonstrated that microRNA (miR)-325-3p expression was significantly increased in both tissues and serum samples of patients with CRC. In addition, miR-325-3p expression in the tissues and serum was significantly associated with differentiation, TNM stage and lymph node metastasis. The results of the dual-luciferase reporter assay and western blot analysis revealed that cytokeratin 18 (CK18) is a target gene of miR-325-3p. Furthermore, treatment with transforming growth factor (TGF)-β increased miR-325-3p expression in a time-dependent manner. Conversely, TGF-β decreased CK18 expression at 48 and 72 h. Western blot analysis demonstrated that TGF-β1 significantly decreased the expression of the epithelial marker, CK18, and increased the expression of the mesenchymal markers, α-SMA and vimentin. Notably, these effects were reversed following inhibition of miR-325-3p expression. Taken together, the results of the present study suggest that miR-325-3p is a key regulator of TGF-β-induced CK18 downregulation. Thus, elevated levels of miR-325-3p is an important factor affecting epithelial-to-mesenchymal transition, and is likely to be a molecular marker in the progression of CRC and act as a potential therapeutic target.Breast cancer (BC) is the leading cause of death in females worldwide. Although cisplatin is a strong-effect and broad-spectrum chemotherapy drug, resistance to cisplatin remains a significant factor effecting clinical efficacy. The underlying mechanism of cancer cell resistance to cisplatin is not fully understood. MicroRNAs (miRs/miRNAs), as a regulator, are involved in regulating chemosensitivity to numerous chemotherapeutic drugs. The present study aimed to investigate the function of miR-181a-5p as a potential tumor suppressor in improving the efficiency of cisplatin in BC. The IC50 of cisplatin and miR-181a-5p expression were determined in five BC cell lines, and HS578T was selected as an appropriate cell line for subsequent experiments. The sensitivity of HS578T cells to cisplatin was assessed using cell proliferation, migration and apoptosis assays. Western blotting was performed to detect the expression of vitamin D receptor (VDR) and autophagy in HS578T cells. It was found that the increase in autophagy resulted in increased apoptosis and sensitivity to cisplatin in HS578T cells.