Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30536 (PBS)
 9,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim was to expound the pathogenesis of prostate cancer and to identify the potentially biomarkers for prostate cancer (PC). DNA methylation microarray data GSE38240 containing 8 prostate cancer metastases and 4 normal prostate samples as well as gene expression profile data GSE26910 containing 6 prostate primary tumors and 6 normal samples were used. Differentially expressed genes (DEGs) and differently methylated sites of PC were screened and the regulatory network was constructed with DEGs-related transcription factors (TFs). The obtained hub genes were subjected to protein-protein interaction network analysis. Enrichment analysis of down-regulated DEGs were performed. Total 351 DEGs including 190 down-regulated and 161 up-regulated genes and 3234 differently methylated sites were identified. In total 69 DEGs-related TFs were found. Regulatory network contained 1301 nodes and 2527 connection pairs and that FOXA1 (forkhead box A1), BZRAP1-AS1 (benzodiazapine receptor associated protein 1 antisense RNA 1) and KRT8 (keratin 8) were the top three nodes of it. The enriched GO terms were mainly biological activity of the blood and cells-related. Total 29 DEGs (such as AGTR1, angiotensin II receptor, type 1) and 57 none-DEGs involved in the PPI network. Biological functions in blood circulation and the involved AGTR1 may play important roles in PC by gene-methylation. Besides, BZRAP1-AS1 may be novel biomarker related with PC.
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PMID:Integrated Bioinformatics Analysis of Potential Biomarkers for Prostate Cancer. 2926 Mar 98

Objective: Recently, the role of long non-coding RNAs (lncRNAs) in hepatocellular carcinoma (HCC) has been assessed. Our research was determined to investigate the impacts of lncRNA TP73-AS1 on radioresistance of HCC by modulating PTEN/Akt signaling pathway. Methods: Expression of TP73-AS1 in HCC tissues and cells was detected using reverse transcription quantitative polymerase chain reaction (RT-qPCR). The HCC cells were conducted with different doses of irradiation, then the survival, colony formation and apoptosis were determined by a series of assays. The HCC cell line with a higher expression of TP73-AS1 was transfected with TP73-AS1-siRNA and X-rayed, the expression of TP73-AS1, cell survival, radiosensitivity, and apoptosis were evaluated. Subcutaneous tumorigenesis in nude mice was adopted to record the size of tumors before and after the radiation. RT-qPCR and Western blot analysis were used to clarify the activation of PTEN/Akt signaling pathway. Results: TP73-AS1 was highly expressed in HCC tissues and cells. With the increasing dose of radiation, the relative proliferation activity and survival fraction (SF) of HCC cells was gradually reduced, while the total apoptosis rate was gradually elevated. TP73-AS1 knockdown promoted radiosensitivity and apoptosis, repressed cell proliferation, making it an inhibitor of tumor in HCC. Moreover, reduced TP73-AS1 was able to decline the phosphorylation of Akt and increase the expression of PTEN in HCC. Down-regulated TP73-AS1 could repress tumorigenesis by promoting radiosensitivity in nude mice with HCC. Conclusion: Our study suggests that lncRNA TP73-AS1 was highly expressed in HCC and participated in radioresistance of HCC via PTEN/Akt signaling pathway. Abbreviations: lncRNAs: long non-coding RNAs; lncRNAs: HCC: hepatocellular carcinoma; RT-qPCR: reverse transcription quantitative polymerase chain reaction; survival fraction: SF; lncRNA TP73-AS1: LncRNA P73 antisense RNA 1T; PTEN: Phosphatase and tensin homologue; Akt: Protein kinase B; P13K: phosphatidylinositol 3-kinase; TNM: tumor, node and metastasis; ACJJ: American Joint Committee on Cancer; FBS: fetal bovine serum; EDTA: ethylene diamine tetraacetic acid; NC: negative control; DMEM: Dulbecco's modified Eagle medium; OD: optical density; PE: Plating efficiency; FITC/PI: fluoresceine isothiocyanate/propidium iodide; PBS: phosphate buffered solution; GAPDH: Glyceraldehyde phosphate dehydrogenase; ANOVA: one-way analysis of variance; LSD-t: least significant difference test.
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PMID:Down-regulated lncRNA TP73-AS1 reduces radioresistance in hepatocellular carcinoma via the PTEN/Akt signaling pathway. 3156 1

Hepatocellular carcinoma (HCC) is recognized for its high mortality rate worldwide. Based on intensive studies, long non-coding RNA (lncRNA) expression exerts significant effects on tumor suppression. Herein, we investigated the molecular mechanism of lymphoid enhancer-binding factor-1 antisense RNA 1 (LEF1-AS1) in HCC cells. Microarray-based gene expression analysis was adopted to predict and verify the differentially expressed genes in HCC, which predicted cell division cycle-associated 7 (CDCA7) and LEF1-AS1 to be highly expressed in HCC. The expression of LEF1-AS1, CDCA7, CCAAT/enhancer-binding protein beta (CEBPB) and enhancer of zeste homolog 2 (EZH2) was determined by means of reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot analysis. LncMap was used to predict the lncRNA-transcription factor-gene interaction in HCC. ChIP, RIP assay and dual luciferase reporter gene assay were employed to verify the relationship between the transcription factor and gene. Silencing of LEF1-AS1 could downregulate CDCA7 expression through CEBPB. Overexpression of LEF1-AS1, EZH2 and CDCA7 promoted proliferation and invasion in HCC cells. LEF1-AS1 promoted CDCA7 expression to further upregulate EZH2. Tumor formation in nude mice was assessed to verify the experimental results. Silencing of LEF1-AS1 inhibited the growth of tumors in vivo. Collectively, silencing LEF1-AS1 inhibited the proliferation and invasion of HCC cells by down-regulating EZH2 through the CEBPB-CDCA7 signaling pathway, which provides scientific evidence for the treatment of HCC.Abbreviations: HCC: Hepatocellular carcinoma; lncRNA: long non-coding RNA; LEF1-AS1: lymphoid enhancer-binding factor-1 antisense RNA 1; EZH2: enhancer of zeste homolog 2; CDCA7: cell division cycle-associated 7; GEO: Gene Expression Omnibus; NC: negative control; oe: overexpressed; RT-qPCR: reverse transcription quantitative polymerase chain reaction; PBS: phosphate buffered saline; HRP: horseradish peroxidase; OD: optical density; RIP: Radioimmunoprecipitation; ChIP: Chromatin immunoprecipitation; WT: wild type.
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PMID:LncRNA LEF1-AS1 silencing diminishes EZH2 expression to delay hepatocellular carcinoma development by impairing CEBPB-interaction with CDCA7. 3217 58