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10.1038/srep11724 http://scihub22266oqcxt.onion/10.1038/srep11724 C4495428!4495428 !26152361     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26152361 &cmd=llinks): Failed to open stream: HTTP request failed! 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Bridging Links between Long Noncoding RNA HOTAIR and HPV Oncoprotein E7 in Cervical Cancer Pathogenesis |pdf=|usr=}}{{26152361 }} gab.com Text Bridging Links between Long Noncoding RNA HOTAIR and HPV Oncoprotein E7 in Cervical Cancer Pathogenesis JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26152361 #FOAvip Human Papillomavirus (HPV) type 16 oncoprotein E7 plays a major role in cervical carcinogenesis by interacting with and functionally inactivating various host regulatory molecules. Long noncoding RNA (lncRNA) HOTAIR is one such regulator that recruits chromatin remodelling complex PRC2, creating gene silencing H3K27?me3 marks. Hence, we hypothesized that HOTAIR could be a potential target of E7, in HPV16 related cervical cancers (CaCx). We identified significant linear trend of progressive HOTAIR down-regulation through HPV negative controls, HPV16 positive non-malignants and CaCx samples. Majority of CaCx cases portrayed HOTAIR down-regulation in comparison to HPV negative controls, with corresponding up-regulation of HOTAIR target, HOXD10, and enrichment of cancer related pathways. However, a small subset had significantly higher HOTAIR expression, concomitant with high E7 expression and enrichment of metastatic pathways. Expression of HOTAIR and PRC2-complex members (EZH2 and SUZ12), showed significant positive correlation with E7 expression in CaCx cases and E7 transfected C33A cell line, suggestive of interplay between E7 and HOTAIR. Functional inactivation of HOTAIR by direct interaction with E7 could also be predicted by in silico analysis and confirmed by RNA-Immunoprecipitation. Our study depicts one of the causal mechanisms of cervical carcinogenesis by HPV16 E7, through modulation of HOTAIR expression and function. Twit Text FOAVip Bridging Links between Long Noncoding RNA HOTAIR and HPV Oncoprotein E7 in Cervical Cancer Pathogenesis ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26152361 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26152361 #FOAvip English Wikipedia <ref>{{Cite pmid|26152361 }}</ref> Bridging Links between Long Noncoding RNA HOTAIR and HPV Oncoprotein E7 in Cervical Cancer Pathogenesis #MMPMID26152361 Sharma S ; Mandal P ; Sadhukhan T ; Roy Chowdhury R ; Ranjan Mondal N ; Chakravarty B ; Chatterjee T ; Roy S ; Sengupta S Sci Rep 2015[Jul]; 5 (ä): 11724 PMID26152361 show ga Human Papillomavirus (HPV) type 16 oncoprotein E7 plays a major role in cervical carcinogenesis by interacting with and functionally inactivating various host regulatory molecules. Long noncoding RNA (lncRNA) HOTAIR is one such regulator that recruits chromatin remodelling complex PRC2, creating gene silencing H3K27?me3 marks. Hence, we hypothesized that HOTAIR could be a potential target of E7, in HPV16 related cervical cancers (CaCx). We identified significant linear trend of progressive HOTAIR down-regulation through HPV negative controls, HPV16 positive non-malignants and CaCx samples. Majority of CaCx cases portrayed HOTAIR down-regulation in comparison to HPV negative controls, with corresponding up-regulation of HOTAIR target, HOXD10, and enrichment of cancer related pathways. However, a small subset had significantly higher HOTAIR expression, concomitant with high E7 expression and enrichment of metastatic pathways. Expression of HOTAIR and PRC2-complex members (EZH2 and SUZ12), showed significant positive correlation with E7 expression in CaCx cases and E7 transfected C33A cell line, suggestive of interplay between E7 and HOTAIR. Functional inactivation of HOTAIR by direct interaction with E7 could also be predicted by in silico analysis and confirmed by RNA-Immunoprecipitation. Our study depicts one of the causal mechanisms of cervical carcinogenesis by HPV16 E7, through modulation of HOTAIR expression and function. |Adult [MESH] |Aged [MESH] |Aged, 80 and over [MESH] |Cell Line, Tumor [MESH] |Down-Regulation [MESH] |Enhancer of Zeste Homolog 2 Protein [MESH] |Female [MESH] |Gene Expression Profiling [MESH] |Histones/metabolism [MESH] |Homeodomain Proteins/genetics/metabolism [MESH] |Human papillomavirus 16/*metabolism [MESH] |Humans [MESH] |Middle Aged [MESH] |Neoplasm Proteins [MESH] |Neoplasm Staging [MESH] |Papillomavirus E7 Proteins/genetics/*metabolism [MESH] |Polycomb Repressive Complex 2/genetics/metabolism [MESH] |RNA, Long Noncoding/genetics/*metabolism [MESH] |ROC Curve [MESH] |Real-Time Polymerase Chain Reaction [MESH] |Transcription Factors/genetics/metabolism [MESH] |Up-Regulation [MESH]Bridging Links between Long Noncoding RNA HOTAIR and HPV Oncoprotein E(epmc).pdf DeepDyve Pubget Overpricing