GSDME with a moonlighting function in pancreatic ductal adenocarcinoma: a narrative review  

作　　者：Bo Huang 

机构地区：[1]Department of Immunology&National Key Laboratory of Medical Molecular Biology,Institute of Basic Medical Sciences,Chinese Academy of Medical Sciences&Peking Union Medical College,Beijing 100005,China [2]Department of Biochemistry&Molecular Biology,Tongji Medical College,Huazhong University of Science&Technology,Wuhan 430030,China

出　　处：《Journal of Pancreatology》2022年第3期83-104,共22页胰腺病学杂志（英文）

基　　金：This work was supported by the National Natural Science Foundation of China(81788101);CAMS Innovation Fund for Medical Sciences(CIFMS)(2021-I2M-1-021).

摘　　要：Pancreatic ductal adenocarcinoma(PDAC)originates in the exocrine pancreas and accounts for 95%of pancreatic cancers,with 5-year survival rates of approximately 10%.Multiple factors are involved in PDAC pathogenesis,including internal genetic alterations and external inflammation-related stimuli.Overflow of exocrine pancreatic enzymes caused by PDAC obstruction inevitably results in autolysis of surrounding normal cells and extracellular matrix,generating tissue damage-related inflammation;however,this process does not cause autolysis of PDAC cells.How tumor cells acquire resistance to pancreatic enzymatic digestion has been ignored for a long time.In this review,we discuss how PDAC cells mobilize gasdermin E,a pore-forming protein,to achieve resistance to autolysis by pancreatic digestive enzymes.

关 键 词：PDAC GSDME MUCINS pancreatic enzymes 

分 类 号：R735.9[医药卫生—肿瘤]