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10.1158/1541-7786.MCR-16-0083 http://scihub22266oqcxt.onion/10.1158/1541-7786.MCR-16-0083 C5107158!5107158 !27624777     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27624777 &cmd=llinks): Failed to open stream: HTTP request failed! 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Inhibition of S-Adenosylmethionine-Dependent Methyltransferase Attenuates TGF?1-Induced EMT and Metastasis in Pancreatic Cancer: Putative Roles of miR-663a and miR-4787-5p |pdf=|usr=}}{{27624777 }} gab.com Text Inhibition of S-Adenosylmethionine-Dependent Methyltransferase Attenuates TGF 1-Induced EMT and Metastasis in Pancreatic Cancer: Putative Roles of miR-663a and miR-4787-5p JO: Mol Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=27624777 #FOAvip The identification of epigenetic reversal agents for use in combination chemotherapies to treat human pancreatic ductal adenocarcinomas (PDAC) remains an unmet clinical need. Pharmacologic inhibitors of Enhancer of Zeste Homolog 2 (EZH2) are emerging as potential histone methylation reversal agents for the treatment of various solid tumors and leukemia; however, the surprisingly small set of mRNA targets identified with EZH2 knockdown suggests novel mechanisms contribute to their antitumorigenic effects. Here, 3-deazaneplanocin-A (DZNep), an inhibitor of S-adenosyl-L-homocysteine hydrolase and EZH2 histone lysine-N-methyltransferase, significantly reprograms noncoding microRNA (miRNA) expression and dampens TGF?1-induced epithelial-to-mesenchymal (EMT) signals in pancreatic cancer. In particular, miR-663a and miR-4787-5p were identified as PDAC-downregulated miRNAs that were reactivated by DZNep to directly target TGF?1 for RNA interference. Lentiviral overexpression of miR-663a and miR-4787-5p reduced TGF?1 synthesis and secretion in PDAC cells and partially phenocopied DZNep's EMT-resisting effects, whereas locked nucleic acid (LNA) antagomiRNAs counteracted them. DZNep, miR-663a, and miR-4787-5p reduced tumor burden in vivo and metastases in an orthotopic mouse pancreatic tumor model. Taken together, these findings suggest the epigenetic reprogramming of miRNAs by synthetic histone methylation reversal agents as a viable approach to attenuate TGF?1-induced EMT features in human PDAC and uncover putative miRNA targets involved in the process. IMPLICATIONS: The findings support the potential for synthetic histone methylation reversal agents to be included in future epigenetic-chemotherapeutic combination therapies for pancreatic cancer. Mol Cancer Res; 14(11); 1124-35. ©2016 AACR. Twit Text FOAVip Inhibition of S-Adenosylmethionine-Dependent Methyltransferase Attenuates TGF 1-Induced EMT and Metastasis in Pancreatic Cancer: Putative Roles of miR-663a and miR-4787-5p ????Mol Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=27624777 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27624777 #FOAvip English Wikipedia <ref>{{Cite pmid|27624777 }}</ref> Inhibition of S-Adenosylmethionine-Dependent Methyltransferase Attenuates TGF?1-Induced EMT and Metastasis in Pancreatic Cancer: Putative Roles of miR-663a and miR-4787-5p #MMPMID27624777 Mody HR ; Hung SW ; AlSaggar M ; Griffin J ; Govindarajan R Mol Cancer Res 2016[Nov]; 14 (11 ): 1124-1135 PMID27624777 show ga The identification of epigenetic reversal agents for use in combination chemotherapies to treat human pancreatic ductal adenocarcinomas (PDAC) remains an unmet clinical need. Pharmacologic inhibitors of Enhancer of Zeste Homolog 2 (EZH2) are emerging as potential histone methylation reversal agents for the treatment of various solid tumors and leukemia; however, the surprisingly small set of mRNA targets identified with EZH2 knockdown suggests novel mechanisms contribute to their antitumorigenic effects. Here, 3-deazaneplanocin-A (DZNep), an inhibitor of S-adenosyl-L-homocysteine hydrolase and EZH2 histone lysine-N-methyltransferase, significantly reprograms noncoding microRNA (miRNA) expression and dampens TGF?1-induced epithelial-to-mesenchymal (EMT) signals in pancreatic cancer. In particular, miR-663a and miR-4787-5p were identified as PDAC-downregulated miRNAs that were reactivated by DZNep to directly target TGF?1 for RNA interference. Lentiviral overexpression of miR-663a and miR-4787-5p reduced TGF?1 synthesis and secretion in PDAC cells and partially phenocopied DZNep's EMT-resisting effects, whereas locked nucleic acid (LNA) antagomiRNAs counteracted them. DZNep, miR-663a, and miR-4787-5p reduced tumor burden in vivo and metastases in an orthotopic mouse pancreatic tumor model. Taken together, these findings suggest the epigenetic reprogramming of miRNAs by synthetic histone methylation reversal agents as a viable approach to attenuate TGF?1-induced EMT features in human PDAC and uncover putative miRNA targets involved in the process. IMPLICATIONS: The findings support the potential for synthetic histone methylation reversal agents to be included in future epigenetic-chemotherapeutic combination therapies for pancreatic cancer. Mol Cancer Res; 14(11); 1124-35. ©2016 AACR. |Adenosine/administration & dosage/*analogs & derivatives/pharmacology [MESH] |Animals [MESH] |Antineoplastic Agents/*administration & dosage/pharmacology [MESH] |Carcinoma, Pancreatic Ductal/*drug therapy/genetics/metabolism/pathology [MESH] |Cell Line, Tumor [MESH] |Cell Movement/drug effects [MESH] |Cell Proliferation/drug effects [MESH] |Down-Regulation [MESH] |Epithelial-Mesenchymal Transition/drug effects [MESH] |Gene Expression Regulation, Neoplastic/drug effects [MESH] |Histones/metabolism [MESH] |Humans [MESH] |Methyltransferases/*antagonists & inhibitors/metabolism [MESH] |Mice [MESH] |MicroRNAs/*genetics [MESH] |Pancreatic Neoplasms/*drug therapy/genetics/metabolism/pathology [MESH] |Transforming Growth Factor beta1/*metabolism [MESH]Inhibition of S-Adenosylmethionine-Dependent Methyltransferase Attenua(epmc).pdf DeepDyve Pubget Overpricing