The dark side of ferroptosis in pancreatic cancer

Jiao Liu, Enyong Dai, Rui Kang, Guido Kroemer, Daolin Tang

Research output: Contribution to journalArticlepeer-review

Abstract

Drug-induced ferroptosis, an iron-dependent regulatory necrosis, has been proposed for the therapy of pancreatic ductal adenocarcinoma. However, genetically engineered mouse models have revealed that high-iron diets or deletion of pancreatic GPX4 (a key repressor of ferroptosis) accelerate the development of mutant Kras-driven PDAC by activating the STING1/TMEM173-dependent DNA sensor pathway. Abbreviations ADM: acinar-to-ductal metaplasia; CGAS: cyclic GMP-AMP synthase; DAMP: damage-associated molecular pattern; GPX4: glutathione peroxidase 4; GEMM: genetically engineered mouse models; PDAC: pancreatic ductal adenocarcinoma; PanIN: pancreatic intraepithelial neoplasia, SLC7A11: solute carrier family 7 member 11; STING1: cGAMP-stimulator of interferon response cGAMP interactor 1; TME: tumor microenvironment; 8-OHG: 8-hydroxy-2ʹ-deoxyguanosine.

Original languageEnglish (US)
Article number1868691
JournalOncoImmunology
Volume10
Issue number1
DOIs
StatePublished - 2021

Keywords

  • DNA damage
  • damp
  • ferroptosis
  • immunity
  • macrophages
  • pancreatic cancer
  • pancreatitis
  • sting1

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Oncology

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