silencing of mir-370 in human cholangiocarcinoma by allelic loss and interleukin-6 induced maternal to paternal epigenotype switch沉默mir - 370在人类胆管癌的等位基因丢失和白细胞介素- 6诱导孕产妇父亲epigenotype开关.pdfVIP

silencing of mir-370 in human cholangiocarcinoma by allelic loss and interleukin-6 induced maternal to paternal epigenotype switch沉默mir - 370在人类胆管癌的等位基因丢失和白细胞介素- 6诱导孕产妇父亲epigenotype开关.pdf

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silencing of mir-370 in human cholangiocarcinoma by allelic loss and interleukin-6 induced maternal to paternal epigenotype switch沉默mir - 370在人类胆管癌的等位基因丢失和白细胞介素- 6诱导孕产妇父亲epigenotype开关

Silencing of miR-370 in Human Cholangiocarcinoma by Allelic Loss and Interleukin-6 Induced Maternal to Paternal Epigenotype Switch 1,2,3 1 4 5 5 Fangmei An , Sumitaka Yamanaka , Sarah Allen , Lewis R. Roberts , Gregory J. Gores , 1 2 1 1 4 Timothy M. Pawlik , Qing Xie , Masaharu Ishida , Esteban Mezey , Anne C. Ferguson-Smith , 1 1 Yuriko Mori , Florin M. Selaru * 1 Division of Gastroenterology and Hepatology, Johns Hopkins Hospital, Baltimore, Maryland, United States of America, 2 Department of Infectious Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China, 3 Department of Gastroenterology, Wuxi People’s Hospital Affiliated to Nanjing Medical University, Wuxi, Jiangsu, China, 4 Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, United Kingdom, 5 Divisions of Gastroenterology and Hepatology, College of Medicine, Mayo Clinic, Rochester, Minnesota, United States of America Abstract Cholangiocarcinoma (CCA) is a highly lethal malignant tumor arising from the biliary tract epithelium. Interleukin-6 (IL-6) is a major mediator of inflammation and contributor to carcinogenesis within the biliary tree. Previous studies suggested that enforced IL-6 contributes to cholangiocarcinogenesis through hypermethylation of several genes implicated in CCA. However, the precise mechanisms of IL-6 effects in CCA remain unclear. We now demonstrate that microRNA (miR)-370 is underexpressed in a large cohort of human CCA vs. normal liver tissues. In

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