Abstract
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.
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