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10.18632/oncotarget.13263 http://scihub22266oqcxt.onion/10.18632/oncotarget.13263 C5348405!5348405 !27845892     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27845892 &cmd=llinks): Failed to open stream: HTTP request failed! 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LncRNA H19 confers chemoresistance in ER?-positive breast cancer through epigenetic silencing of the pro-apoptotic gene BIK |pdf=|usr=}}{{27845892 }} gab.com Text LncRNA H19 confers chemoresistance in ER -positive breast cancer through epigenetic silencing of the pro-apoptotic gene BIK JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27845892 #FOAvip Breast cancer is a common malignancy in women. Acquisition of drug resistance is one of the main obstacles encountered in breast cancer therapy. Long non-coding RNA (lncRNA) has been demonstrated to play vital roles in both development and tumorigenesis. However, the relationship between lncRNAs and the development of chemoresistance is not well established. In the present study, the high expression of lncRNA H19 was identified as a powerful factor associated with paclitaxel (PTX) resistance in ER?-positive breast cancer cells, but not in ER?-negative breast cancer cells. LncRNA H19 attenuated cell apoptosis in response to PTX treatment by inhibiting transcription of pro-apoptotic genes BIK and NOXA. H19 was further confirmed to suppress the promoter activity of BIK by recruiting EZH2 and by trimethylating the histone H3 at lysine 27. Interestingly, our data showed that lncRNA H19 was one of the downstream target molecules of ER?. Altered ER? expression may therefore change H19 levels to modulate the apoptosis response to chemotherapy in breast cancer cells. Our data suggest that the ER?-H19-BIK signaling axis plays an important role in promoting chemoresistance. Twit Text FOAVip LncRNA H19 confers chemoresistance in ER -positive breast cancer through epigenetic silencing of the pro-apoptotic gene BIK ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27845892 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27845892 #FOAvip English Wikipedia <ref>{{Cite pmid|27845892 }}</ref> LncRNA H19 confers chemoresistance in ER?-positive breast cancer through epigenetic silencing of the pro-apoptotic gene BIK #MMPMID27845892 Si X ; Zang R ; Zhang E ; Liu Y ; Shi X ; Zhang E ; Shao L ; Li A ; Yang N ; Han X ; Pan B ; Zhang Z ; Sun L ; Sun Y Oncotarget 2016[Dec]; 7 (49 ): 81452-81462 PMID27845892 show ga Breast cancer is a common malignancy in women. Acquisition of drug resistance is one of the main obstacles encountered in breast cancer therapy. Long non-coding RNA (lncRNA) has been demonstrated to play vital roles in both development and tumorigenesis. However, the relationship between lncRNAs and the development of chemoresistance is not well established. In the present study, the high expression of lncRNA H19 was identified as a powerful factor associated with paclitaxel (PTX) resistance in ER?-positive breast cancer cells, but not in ER?-negative breast cancer cells. LncRNA H19 attenuated cell apoptosis in response to PTX treatment by inhibiting transcription of pro-apoptotic genes BIK and NOXA. H19 was further confirmed to suppress the promoter activity of BIK by recruiting EZH2 and by trimethylating the histone H3 at lysine 27. Interestingly, our data showed that lncRNA H19 was one of the downstream target molecules of ER?. Altered ER? expression may therefore change H19 levels to modulate the apoptosis response to chemotherapy in breast cancer cells. Our data suggest that the ER?-H19-BIK signaling axis plays an important role in promoting chemoresistance. |*DNA Methylation [MESH] |*Epigenesis, Genetic [MESH] |Antineoplastic Agents/*pharmacology [MESH] |Apoptosis Regulatory Proteins/*genetics/metabolism [MESH] |Apoptosis/*drug effects [MESH] |Breast Neoplasms/*drug therapy/*genetics/metabolism/pathology [MESH] |Dose-Response Relationship, Drug [MESH] |Drug Resistance, Neoplasm/*genetics [MESH] |Enhancer of Zeste Homolog 2 Protein/genetics/metabolism [MESH] |Estrogen Receptor alpha/drug effects/*metabolism [MESH] |Female [MESH] |Gene Expression Regulation, Neoplastic [MESH] |Humans [MESH] |MCF-7 Cells [MESH] |Membrane Proteins/*genetics/metabolism [MESH] |Mitochondrial Proteins [MESH] |Paclitaxel/*pharmacology [MESH] |Proto-Oncogene Proteins c-bcl-2/genetics/metabolism [MESH] |RNA Interference [MESH] |RNA, Long Noncoding/*genetics/metabolism [MESH] |Signal Transduction [MESH] |Transcription, Genetic [MESH]LncRNA H19 confers chemoresistance in ER?-positive breast cancer throu(epmc).pdf DeepDyve Pubget Overpricing