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10.1038/s41419-018-0807-3 http://scihub22266oqcxt.onion/10.1038/s41419-018-0807-3 C6045651!6045651 !30006541     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=30006541 &cmd=llinks): Failed to open stream: HTTP request failed! 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Transcriptional downregulation of miR-133b by REST promotes prostate cancer metastasis to bone via activating TGF-? signaling |pdf=|usr=}}{{30006541 }} gab.com Text Transcriptional downregulation of miR-133b by REST promotes prostate cancer metastasis to bone via activating TGF- signaling JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=30006541 #FOAvip High avidity of bone metastasis is an important characteristic in prostate cancer (PCa). Downexpression of miR-133b has been reported to be implicated in the development, progression and recurrence in PCa. However, clinical significance and biological roles of miR-133b in bone metastasis of PCa remain unclear. Here we report that miR-133b is downregulated in PCa tissues and further decreased in bone metastatic PCa tissues. Downexpression of miR-133b positively correlates with advanced clinicopathological characteristics and shorter bone metastasis-free survival in PCa patients. Upregulating miR-133b inhibits invasion, migration in vitro and bone metastasis in vivo in PCa cells. Mechanistically, we find that miR-133b suppresses activity of TGF-? signaling via directly targeting TGF-? receptor I and II, which further inhibits bone metastasis of PCa cells. Our results further reveal that overexpression of REST contributes to miR-133b downexpression via transcriptional repression in PCa tissues. Importantly, silencing miR-133b enhances invasion and migration abilities in vitro and bone metastasis ability in vivo in REST-silenced PCa cells. The clinical correlation of miR-133b with TGFBRI, TGFBRII, REST and TGF-? signaling activity is verified in PCa tissues. Therefore, our results uncover a novel mechanism of miR-133b downexpression that REST transcriptionally inhibits miR-133b expression in PCa cells, and meanwhile support the notion that administration of miR-133b may serve as a rational regimen in the treatment of PCa bone metastasis. Twit Text FOAVip Transcriptional downregulation of miR-133b by REST promotes prostate cancer metastasis to bone via activating TGF- signaling ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=30006541 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30006541 #FOAvip English Wikipedia <ref>{{Cite pmid|30006541 }}</ref> Transcriptional downregulation of miR-133b by REST promotes prostate cancer metastasis to bone via activating TGF-? signaling #MMPMID30006541 Huang S ; Wa Q ; Pan J ; Peng X ; Ren D ; Li Q ; Dai Y ; Yang Q ; Huang Y ; Zhang X ; Zhou W ; Yuan D ; Cao J ; Li Y ; He P ; Tang Y Cell Death Dis 2018[Jul]; 9 (7 ): 779 PMID30006541 show ga High avidity of bone metastasis is an important characteristic in prostate cancer (PCa). Downexpression of miR-133b has been reported to be implicated in the development, progression and recurrence in PCa. However, clinical significance and biological roles of miR-133b in bone metastasis of PCa remain unclear. Here we report that miR-133b is downregulated in PCa tissues and further decreased in bone metastatic PCa tissues. Downexpression of miR-133b positively correlates with advanced clinicopathological characteristics and shorter bone metastasis-free survival in PCa patients. Upregulating miR-133b inhibits invasion, migration in vitro and bone metastasis in vivo in PCa cells. Mechanistically, we find that miR-133b suppresses activity of TGF-? signaling via directly targeting TGF-? receptor I and II, which further inhibits bone metastasis of PCa cells. Our results further reveal that overexpression of REST contributes to miR-133b downexpression via transcriptional repression in PCa tissues. Importantly, silencing miR-133b enhances invasion and migration abilities in vitro and bone metastasis ability in vivo in REST-silenced PCa cells. The clinical correlation of miR-133b with TGFBRI, TGFBRII, REST and TGF-? signaling activity is verified in PCa tissues. Therefore, our results uncover a novel mechanism of miR-133b downexpression that REST transcriptionally inhibits miR-133b expression in PCa cells, and meanwhile support the notion that administration of miR-133b may serve as a rational regimen in the treatment of PCa bone metastasis. |*Signal Transduction [MESH] |*Transcription, Genetic [MESH] |Animals [MESH] |Bone Neoplasms/*secondary [MESH] |Cell Line, Tumor [MESH] |Down-Regulation/*genetics [MESH] |Gene Expression Regulation, Neoplastic [MESH] |Humans [MESH] |Male [MESH] |Mice, Inbred BALB C [MESH] |Mice, Nude [MESH] |MicroRNAs/*genetics/metabolism [MESH] |Prostatic Neoplasms/*genetics [MESH] |Receptors, Transforming Growth Factor beta/metabolism [MESH] |Repressor Proteins/*metabolism [MESH]Transcriptional downregulation of miR-133b by REST promotes prostate c(epmc).pdf DeepDyve Pubget Overpricing