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10.1158/0008-5472.CAN-15-3264 http://scihub22266oqcxt.onion/10.1158/0008-5472.CAN-15-3264 C5026619!5026619 !27496707     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27496707 &cmd=llinks): Failed to open stream: HTTP request failed! 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Cancer-Associated Fibroblasts in Pancreatic Cancer Are Reprogrammed by Tumor-Induced Alterations in Genomic DNA Methylation |pdf=|usr=}}{{27496707 }} gab.com Text Cancer-Associated Fibroblasts in Pancreatic Cancer Are Reprogrammed by Tumor-Induced Alterations in Genomic DNA Methylation JO: Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=27496707 #FOAvip Stromal fibrosis is a prominent histologic characteristic of pancreatic ductal adenocarcinoma (PDAC), but how stromal fibroblasts are regulated in the tumor microenvironment (TME) to support tumor growth is largely unknown. Here we show that PDAC cells can induce DNA methylation in cancer-associated fibroblasts (CAF). Upon direct contact with PDAC cells, DNA methylation of SOCS1 and other genes is induced in mesenchymal stem cells or in CAF that lack SOCS1 methylation at baseline. Silencing or decitabine treatment to block the DNA methylation enzyme DNMT1 inhibited methylation of SOCS1. In contrast, SOCS1 gene methylation and downregulation in CAF activated STAT3 and induced insulin-like growth factor-1 expression to support PDAC cell growth. Moreover, CAF facilitated methylation-dependent growth of PDAC tumor xenografts in mice. The ability of patient-derived CAF with SOCS1 methylation to promote PDAC growth was more robust than CAF without SOCS1 methylation. Overall, our results reveal how PDAC cells can reprogram CAF to modify tumor-stromal interactions in the TME, which promote malignant growth and progression. Cancer Res; 76(18); 5395-404. ©2016 AACR. Twit Text FOAVip Cancer-Associated Fibroblasts in Pancreatic Cancer Are Reprogrammed by Tumor-Induced Alterations in Genomic DNA Methylation ????Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=27496707 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27496707 #FOAvip English Wikipedia <ref>{{Cite pmid|27496707 }}</ref> Cancer-Associated Fibroblasts in Pancreatic Cancer Are Reprogrammed by Tumor-Induced Alterations in Genomic DNA Methylation #MMPMID27496707 Xiao Q ; Zhou D ; Rucki AA ; Williams J ; Zhou J ; Mo G ; Murphy A ; Fujiwara K ; Kleponis J ; Salman B ; Wolfgang CL ; Anders RA ; Zheng S ; Jaffee EM ; Zheng L Cancer Res 2016[Sep]; 76 (18 ): 5395-404 PMID27496707 show ga Stromal fibrosis is a prominent histologic characteristic of pancreatic ductal adenocarcinoma (PDAC), but how stromal fibroblasts are regulated in the tumor microenvironment (TME) to support tumor growth is largely unknown. Here we show that PDAC cells can induce DNA methylation in cancer-associated fibroblasts (CAF). Upon direct contact with PDAC cells, DNA methylation of SOCS1 and other genes is induced in mesenchymal stem cells or in CAF that lack SOCS1 methylation at baseline. Silencing or decitabine treatment to block the DNA methylation enzyme DNMT1 inhibited methylation of SOCS1. In contrast, SOCS1 gene methylation and downregulation in CAF activated STAT3 and induced insulin-like growth factor-1 expression to support PDAC cell growth. Moreover, CAF facilitated methylation-dependent growth of PDAC tumor xenografts in mice. The ability of patient-derived CAF with SOCS1 methylation to promote PDAC growth was more robust than CAF without SOCS1 methylation. Overall, our results reveal how PDAC cells can reprogram CAF to modify tumor-stromal interactions in the TME, which promote malignant growth and progression. Cancer Res; 76(18); 5395-404. ©2016 AACR. |Animals [MESH] |Cancer-Associated Fibroblasts/*pathology [MESH] |Carcinoma, Pancreatic Ductal/*genetics/pathology [MESH] |DNA Methylation/*genetics [MESH] |Heterografts [MESH] |Humans [MESH] |Mice [MESH] |Mice, Inbred NOD [MESH] |Mice, SCID [MESH] |Oligonucleotide Array Sequence Analysis [MESH] |Pancreatic Neoplasms/*genetics/pathology [MESH] |Polymerase Chain Reaction [MESH] |Suppressor of Cytokine Signaling 1 Protein/*genetics [MESH]Cancer-Associated Fibroblasts in Pancreatic Cancer Are Reprogrammed by(epmc).pdf DeepDyve Pubget Overpricing