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10.1038/cddis.2015.150 http://scihub22266oqcxt.onion/10.1038/cddis.2015.150 C4650715!4650715 !26136075     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26136075 &cmd=llinks): Failed to open stream: HTTP request failed! 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LincHOTAIR epigenetically silences miR34a by binding to PRC2 to promote the epithelial-to-mesenchymal transition in human gastric cancer |pdf=|usr=}}{{26136075 }} gab.com Text LincHOTAIR epigenetically silences miR34a by binding to PRC2 to promote the epithelial-to-mesenchymal transition in human gastric cancer JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=26136075 #FOAvip lncRNAs play important roles in the epigenetic regulation of carcinogenesis and progression. Previous studies suggest that HOTAIR contributes to gastric cancer (GC) development, and the overexpression of HOTAIR predicts a poor prognosis. In this study, we found that HOTAIR was more highly expressed in diffuse-type GC than in intestinal type (P=0.048). In the diffuse type, there is significant relationship between HOTAIR expression and DFS (P<0.001). CDH1 was downregulated in diffuse-type GC tissues (P=0.0007) and showed a negative relationship with HOTAIR (r(2)=0.154, P=0.0354). In addition, HOTAIR knockdown significantly repressed migration, invasion and metastasis both in vitro and vivo and reversed the epithelial-to-mesenchymal transition in GC cells. We also showed that HOTAIR recruiting and binding to PRC2 epigenetically represses miR34a, which controls the targets C-Met (HGF/C-Met/Snail pathway) and Snail, thus contributing to GC cell-EMT process and accelerating tumor metastasis. Moreover, it is demonstrated that HOTAIR crosstalk with microRNAs during epigenetic regulation. Our results suggest that HOTAIR acts as an EMT regulator and may be a candidate prognostic biomarker and a target for new therapies in GC patients. Twit Text FOAVip LincHOTAIR epigenetically silences miR34a by binding to PRC2 to promote the epithelial-to-mesenchymal transition in human gastric cancer ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=26136075 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26136075 #FOAvip English Wikipedia <ref>{{Cite pmid|26136075 }}</ref> LincHOTAIR epigenetically silences miR34a by binding to PRC2 to promote the epithelial-to-mesenchymal transition in human gastric cancer #MMPMID26136075 Liu YW ; Sun M ; Xia R ; Zhang EB ; Liu XH ; Zhang ZH ; Xu TP ; De W ; Liu BR ; Wang ZX Cell Death Dis 2015[Jul]; 6 (7 ): e1802 PMID26136075 show ga lncRNAs play important roles in the epigenetic regulation of carcinogenesis and progression. Previous studies suggest that HOTAIR contributes to gastric cancer (GC) development, and the overexpression of HOTAIR predicts a poor prognosis. In this study, we found that HOTAIR was more highly expressed in diffuse-type GC than in intestinal type (P=0.048). In the diffuse type, there is significant relationship between HOTAIR expression and DFS (P<0.001). CDH1 was downregulated in diffuse-type GC tissues (P=0.0007) and showed a negative relationship with HOTAIR (r(2)=0.154, P=0.0354). In addition, HOTAIR knockdown significantly repressed migration, invasion and metastasis both in vitro and vivo and reversed the epithelial-to-mesenchymal transition in GC cells. We also showed that HOTAIR recruiting and binding to PRC2 epigenetically represses miR34a, which controls the targets C-Met (HGF/C-Met/Snail pathway) and Snail, thus contributing to GC cell-EMT process and accelerating tumor metastasis. Moreover, it is demonstrated that HOTAIR crosstalk with microRNAs during epigenetic regulation. Our results suggest that HOTAIR acts as an EMT regulator and may be a candidate prognostic biomarker and a target for new therapies in GC patients. |Animals [MESH] |Antigens, CD [MESH] |Biomarkers, Tumor/genetics [MESH] |Cadherins/biosynthesis [MESH] |Cell Line, Tumor [MESH] |Cell Movement/genetics [MESH] |Down-Regulation/genetics [MESH] |Enhancer of Zeste Homolog 2 Protein [MESH] |Epithelial-Mesenchymal Transition/*genetics [MESH] |Gene Expression Regulation, Neoplastic [MESH] |Gene Silencing [MESH] |Histones/genetics [MESH] |Humans [MESH] |Male [MESH] |Mice [MESH] |Mice, Nude [MESH] |MicroRNAs/*genetics [MESH] |Neoplasm Invasiveness/genetics [MESH] |Neoplasm Metastasis/genetics [MESH] |Neoplasm Proteins [MESH] |Polycomb Repressive Complex 2/genetics [MESH] |Promoter Regions, Genetic/genetics [MESH] |RNA Interference [MESH] |RNA, Long Noncoding/*genetics [MESH] |RNA, Small Interfering [MESH] |Snail Family Transcription Factors [MESH] |Stomach Neoplasms/*genetics/pathology [MESH]LincHOTAIR epigenetically silences miR34a by binding to PRC2 to promot(epmc).pdf DeepDyve Pubget Overpricing