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10.1038/cddis.2016.438 http://scihub22266oqcxt.onion/10.1038/cddis.2016.438 C5386357!5386357 !28102845     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28102845 &cmd=llinks): Failed to open stream: HTTP request failed! 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H19/let-7/LIN28 reciprocal negative regulatory circuit promotes breast cancer stem cell maintenance |pdf=|usr=}}{{28102845 }} gab.com Text H19/let-7/LIN28 reciprocal negative regulatory circuit promotes breast cancer stem cell maintenance JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=28102845 #FOAvip Long noncoding RNA-H19 (H19), an imprinted oncofetal gene, has a central role in carcinogenesis. Hitherto, the mechanism by which H19 regulates cancer stem cells, remains elusive. Here we show that breast cancer stem cells (BCSCs) express high levels of H19, and ectopic overexpression of H19 significantly promotes breast cancer cell clonogenicity, migration and mammosphere-forming ability. Conversely, silencing of H19 represses these BCSC properties. In concordance, knockdown of H19 markedly inhibits tumor growth and suppresses tumorigenesis in nude mice. Mechanistically, we found that H19 functions as a competing endogenous RNA to sponge miRNA let-7, leading to an increase in expression of a let-7 target, the core pluripotency factor LIN28, which is enriched in BCSC populations and breast patient samples. Intriguingly, this gain of LIN28 expression can also feedback to reverse the H19 loss-mediated suppression of BCSC properties. Our data also reveal that LIN28 blocks mature let-7 production and, thereby, de-represses H19 expression in breast cancer cells. Appropriately, H19 and LIN28 expression exhibits strong correlations in primary breast carcinomas. Collectively, these findings reveal that lncRNA H19, miRNA let-7 and transcriptional factor LIN28 form a double-negative feedback loop, which has a critical role in the maintenance of BCSCs. Consequently, disrupting this pathway provides a novel therapeutic strategy for breast cancer. Twit Text FOAVip H19/let-7/LIN28 reciprocal negative regulatory circuit promotes breast cancer stem cell maintenance ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=28102845 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28102845 #FOAvip English Wikipedia <ref>{{Cite pmid|28102845 }}</ref> H19/let-7/LIN28 reciprocal negative regulatory circuit promotes breast cancer stem cell maintenance #MMPMID28102845 Peng F ; Li TT ; Wang KL ; Xiao GQ ; Wang JH ; Zhao HD ; Kang ZJ ; Fan WJ ; Zhu LL ; Li M ; Cui B ; Zheng FM ; Wang HJ ; Lam EW ; Wang B ; Xu J ; Liu Q Cell Death Dis 2017[Jan]; 8 (1 ): e2569 PMID28102845 show ga Long noncoding RNA-H19 (H19), an imprinted oncofetal gene, has a central role in carcinogenesis. Hitherto, the mechanism by which H19 regulates cancer stem cells, remains elusive. Here we show that breast cancer stem cells (BCSCs) express high levels of H19, and ectopic overexpression of H19 significantly promotes breast cancer cell clonogenicity, migration and mammosphere-forming ability. Conversely, silencing of H19 represses these BCSC properties. In concordance, knockdown of H19 markedly inhibits tumor growth and suppresses tumorigenesis in nude mice. Mechanistically, we found that H19 functions as a competing endogenous RNA to sponge miRNA let-7, leading to an increase in expression of a let-7 target, the core pluripotency factor LIN28, which is enriched in BCSC populations and breast patient samples. Intriguingly, this gain of LIN28 expression can also feedback to reverse the H19 loss-mediated suppression of BCSC properties. Our data also reveal that LIN28 blocks mature let-7 production and, thereby, de-represses H19 expression in breast cancer cells. Appropriately, H19 and LIN28 expression exhibits strong correlations in primary breast carcinomas. Collectively, these findings reveal that lncRNA H19, miRNA let-7 and transcriptional factor LIN28 form a double-negative feedback loop, which has a critical role in the maintenance of BCSCs. Consequently, disrupting this pathway provides a novel therapeutic strategy for breast cancer. |Breast Neoplasms/*genetics/pathology [MESH] |Carcinogenesis/genetics [MESH] |Cell Line, Tumor [MESH] |Female [MESH] |Gene Expression Regulation, Neoplastic [MESH] |Humans [MESH] |MicroRNAs/biosynthesis/*genetics [MESH] |Neoplastic Stem Cells/metabolism/pathology [MESH] |RNA, Long Noncoding/biosynthesis/*genetics [MESH]H19/let-7/LIN28 reciprocal negative regulatory circuit promotes breast(epmc).pdf DeepDyve Pubget Overpricing