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10.1186/s12943-015-0431-0 http://scihub22266oqcxt.onion/10.1186/s12943-015-0431-0 C4558931!4558931 !26336870     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26336870 &cmd=llinks): Failed to open stream: HTTP request failed! 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Long non-coding RNA TUG1 is up-regulated in hepatocellular carcinoma and promotes cell growth and apoptosis by epigenetically silencing of KLF2 |pdf=|usr=}}{{26336870 }} gab.com Text Long non-coding RNA TUG1 is up-regulated in hepatocellular carcinoma and promotes cell growth and apoptosis by epigenetically silencing of KLF2 JO: Mol Cancer http://www.kidney.de/pget.php?&tw=1&pmid=26336870 #FOAvip BACKGROUND: Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related death worldwide, and the biology of this cancer remains poorly understood. Recent evidence indicates that long non-coding RNAs (lncRNAs) are found to be dysregulated in a variety of cancers, including HCC. Taurine Up-regulated Gene 1 (TUG1), a 7.1-kb lncRNA, recruiting and binding to polycomb repressive complex 2 (PRC2), is found to be disregulated in non-small cell lung carcinoma (NSCLC) and esophageal squamous cell carcinoma (ESCC). However, its clinical significance and potential role in HCC remain unclear. METHODS AND RESULTS: In this study, expression of TUG1 was analyzed in 77 HCC tissues and matched normal tissues by using quantitative polymerase chain reaction (qPCR). TUG1 expression was up-regulated in HCC tissues and the higher expression of TUG1 was significantly correlated with tumor size and Barcelona Clinic Liver Cancer (BCLC) stage. Moreover, silencing of TUG1 expression inhibited HCC cell proliferation, colony formation, tumorigenicity and induced apoptosis in HCC cell lines. We also found that TUG1 overexpression was induced by nuclear transcription factor SP1 and TUG1 could epigeneticly repress Kruppel-like factor 2 (KLF2) transcription in HCC cells by binding with PRC2 and recruiting it to KLF2 promoter region. CONCLUSION: Our results suggest that lncRNA TUG1, as a growth regulator, may serve as a new diagnostic biomarker and therapy target for HCC. Twit Text FOAVip Long non-coding RNA TUG1 is up-regulated in hepatocellular carcinoma and promotes cell growth and apoptosis by epigenetically silencing of KLF2 ????Mol Cancer http://www.kidney.de/pget.php?&tw=1&pmid=26336870 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26336870 #FOAvip English Wikipedia <ref>{{Cite pmid|26336870 }}</ref> Long non-coding RNA TUG1 is up-regulated in hepatocellular carcinoma and promotes cell growth and apoptosis by epigenetically silencing of KLF2 #MMPMID26336870 Huang MD ; Chen WM ; Qi FZ ; Sun M ; Xu TP ; Ma P ; Shu YQ Mol Cancer 2015[Sep]; 14 (ä): 165 PMID26336870 show ga BACKGROUND: Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related death worldwide, and the biology of this cancer remains poorly understood. Recent evidence indicates that long non-coding RNAs (lncRNAs) are found to be dysregulated in a variety of cancers, including HCC. Taurine Up-regulated Gene 1 (TUG1), a 7.1-kb lncRNA, recruiting and binding to polycomb repressive complex 2 (PRC2), is found to be disregulated in non-small cell lung carcinoma (NSCLC) and esophageal squamous cell carcinoma (ESCC). However, its clinical significance and potential role in HCC remain unclear. METHODS AND RESULTS: In this study, expression of TUG1 was analyzed in 77 HCC tissues and matched normal tissues by using quantitative polymerase chain reaction (qPCR). TUG1 expression was up-regulated in HCC tissues and the higher expression of TUG1 was significantly correlated with tumor size and Barcelona Clinic Liver Cancer (BCLC) stage. Moreover, silencing of TUG1 expression inhibited HCC cell proliferation, colony formation, tumorigenicity and induced apoptosis in HCC cell lines. We also found that TUG1 overexpression was induced by nuclear transcription factor SP1 and TUG1 could epigeneticly repress Kruppel-like factor 2 (KLF2) transcription in HCC cells by binding with PRC2 and recruiting it to KLF2 promoter region. CONCLUSION: Our results suggest that lncRNA TUG1, as a growth regulator, may serve as a new diagnostic biomarker and therapy target for HCC. |Adult [MESH] |Aged [MESH] |Apoptosis/genetics [MESH] |Carcinoma, Hepatocellular/*genetics/pathology [MESH] |Cell Proliferation/genetics [MESH] |DNA Methylation/genetics [MESH] |Epigenetic Repression/genetics [MESH] |Female [MESH] |Gene Expression Regulation, Neoplastic [MESH] |Gene Knockdown Techniques [MESH] |Hep G2 Cells [MESH] |Humans [MESH] |Kruppel-Like Transcription Factors/biosynthesis/*genetics [MESH] |Liver Neoplasms/*genetics/pathology [MESH] |Male [MESH] |Middle Aged [MESH] |Polycomb Repressive Complex 2/genetics [MESH] |Promoter Regions, Genetic [MESH]Long non-coding RNA TUG1 is up-regulated in hepatocellular carcinoma a(epmc).pdf DeepDyve Pubget Overpricing