Статья

EZH2 couples pancreatic regeneration to neoplastic progression

Jon Mallen‐St. ClairDepartment of Biochemistry, New York University School of Medicine, New York, NY 10016, USARengin G. Soydaner-AzelogluDepartment of Biochemistry, New York University School of Medicine, New York, New York 10016, USA;Kyoung Eun LeeDepartment of Biochemistry, New York University School of Medicine, New York, New York 10016, USA;Laura TaylorDepartment of Biochemistry, New York University School of Medicine, New York, New York 10016, USA;Alexandra E. LivanosNew York University School of Medicine, New York, New York 10016, USA;Yuliya Pylayeva‐GuptaDepartment of Biochemistry, New York University School of Medicine, New York, New York 10016, USA;George MillerDepartment of Surgery, New York University School of Medicine, New York, New York 10016, USA;Raphaël MargueronDepartment of Biochemistry, New York University School of Medicine, New York, New York 10016, USA;Danny ReinbergDepartment of Biochemistry, New York University School of Medicine, New York, New York 10016, USA;Dafna Bar‐SagiDepartment of Biochemistry, New York University School of Medicine, New York, New York 10016, USA;

2012en

ABI

Аннотация

Although the polycomb group protein Enhancer of Zeste Homolog 2 (EZH2) is well recognized for its role as a key regulator of cell differentiation, its involvement in tissue regeneration is largely unknown. Here we show that EZH2 is up-regulated following cerulein-induced pancreatic injury and is required for tissue repair by promoting the regenerative proliferation of progenitor cells. Loss of EZH2 results in impaired pancreatic regeneration and accelerates KRas(G12D)-driven neoplasia. Our findings implicate EZH2 in constraining neoplastic progression through homeostatic mechanisms that control pancreatic regeneration and provide insights into the documented link between chronic pancreatic injury and an increased risk for pancreatic cancer.

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Идентификаторы

DOI: 10.1101/gad.181800.111

Цитирования и источники

Цитирований: 2Использованных источников: 0

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