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10.18632/oncotarget.6717 http://scihub22266oqcxt.onion/10.18632/oncotarget.6717 C4905483!4905483 !26716510     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26716510 &cmd=llinks): Failed to open stream: HTTP request failed! 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Polycomb repressor complex 1 promotes gene silencing through H2AK119 mono-ubiquitination in acinar-to-ductal metaplasia and pancreatic cancer cells |pdf=|usr=}}{{26716510 }} gab.com Text Polycomb repressor complex 1 promotes gene silencing through H2AK119 mono-ubiquitination in acinar-to-ductal metaplasia and pancreatic cancer cells JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26716510 #FOAvip Acinar-to-ductal metaplasia (ADM) occurring in cerulein-mediated pancreatitis or in oncogenic Kras-driven pancreatic cancer development is accompanied by extensive changes in the transcriptional program. In this process, acinar cells shut down the expression of acinar specific differentiation genes and re-express genes usually found in embryonic pancreatic progenitor cells. Previous studies have demonstrated that a loss of acinar-specific transcription factors sensitizes the cells towards oncogenic transformation, ultimately resulting in cancer development. However, the mechanism behind the transcriptional silencing of acinar cell fate genes in ADM and pancreatic cancer is largely unknown. Here, we analyzed whether elevated levels of the polycomb repressor complex 1 (PRC1) components Bmi1 and Ring1b and their catalyzed histone modification H2AK119ub in ADMs and tumor cells, are responsible for the mediation of acinar gene silencing. Therefore, we performed chromatin-immunoprecipitation in in vitro generated ADMs and isolated murine tumor cells against the repressive histone modifications H3K27me3 and H2AK119ub. We established that the acinar transcription factor complex Ptf1-L is epigenetically silenced in ADMs as well as in pancreatic tumor cells. For the first time, this work presents a possible mechanism of acinar gene silencing, which is an important prerequisite in the initiation and maintenance of a dedifferentiated cell state in ADMs and tumor cells. Twit Text FOAVip Polycomb repressor complex 1 promotes gene silencing through H2AK119 mono-ubiquitination in acinar-to-ductal metaplasia and pancreatic cancer cells ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26716510 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26716510 #FOAvip English Wikipedia <ref>{{Cite pmid|26716510 }}</ref> Polycomb repressor complex 1 promotes gene silencing through H2AK119 mono-ubiquitination in acinar-to-ductal metaplasia and pancreatic cancer cells #MMPMID26716510 Benitz S ; Regel I ; Reinhard T ; Popp A ; Schäffer I ; Raulefs S ; Kong B ; Esposito I ; Michalski CW ; Kleeff J Oncotarget 2016[Mar]; 7 (10 ): 11424-33 PMID26716510 show ga Acinar-to-ductal metaplasia (ADM) occurring in cerulein-mediated pancreatitis or in oncogenic Kras-driven pancreatic cancer development is accompanied by extensive changes in the transcriptional program. In this process, acinar cells shut down the expression of acinar specific differentiation genes and re-express genes usually found in embryonic pancreatic progenitor cells. Previous studies have demonstrated that a loss of acinar-specific transcription factors sensitizes the cells towards oncogenic transformation, ultimately resulting in cancer development. However, the mechanism behind the transcriptional silencing of acinar cell fate genes in ADM and pancreatic cancer is largely unknown. Here, we analyzed whether elevated levels of the polycomb repressor complex 1 (PRC1) components Bmi1 and Ring1b and their catalyzed histone modification H2AK119ub in ADMs and tumor cells, are responsible for the mediation of acinar gene silencing. Therefore, we performed chromatin-immunoprecipitation in in vitro generated ADMs and isolated murine tumor cells against the repressive histone modifications H3K27me3 and H2AK119ub. We established that the acinar transcription factor complex Ptf1-L is epigenetically silenced in ADMs as well as in pancreatic tumor cells. For the first time, this work presents a possible mechanism of acinar gene silencing, which is an important prerequisite in the initiation and maintenance of a dedifferentiated cell state in ADMs and tumor cells. |Animals [MESH] |Carcinoma, Pancreatic Ductal/*genetics/metabolism/pathology [MESH] |Cell Dedifferentiation/genetics [MESH] |Cell Line, Tumor [MESH] |Gene Silencing [MESH] |Histones/*genetics/metabolism [MESH] |Immunohistochemistry [MESH] |Metaplasia/pathology [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Pancreatic Neoplasms/*genetics/metabolism/pathology [MESH] |Polycomb Repressive Complex 1/*genetics/metabolism [MESH] |Signal Transduction [MESH] |Transcription Factors/genetics/metabolism [MESH]Polycomb repressor complex 1 promotes gene silencing through H2AK119 (epmc).pdf DeepDyve Pubget Overpricing