The dark side of ferroptosis in pancreatic cancer

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

    Research output: Contribution to journalArticlepeer-review

    28 Citations (Scopus)

    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
    Article number1868691
    JournalOncoImmunology
    Volume10
    Issue number1
    DOIs
    Publication statusPublished - 1 Jan 2021

    Keywords

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

    Cite this