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

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 stimul...

Full description

Saved in:
Bibliographic Details
Published inJournal of Pancreatology Vol. 5; no. 4; pp. 198 - 201
Main Author Bo Huang
Format Journal Article
LanguageEnglish
Published Wolters Kluwer Health/LWW 01.12.2022
Online AccessGet full text

Cover

More Information
Summary: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.
ISSN:2096-5664
DOI:10.1097/JP9.0000000000000104