IL15RA-STAT3-GPX4/ACSL3 signaling leads to ferroptosis resistance in pancreatic cancer

胰腺癌 癌症研究 GPX4 车站3 生物 信号转导 癌症 遗传学 过氧化氢酶 内分泌学 氧化应激 谷胱甘肽过氧化物酶
作者
Di Wu,Zhiliang Wang,Yue Zhang,Yang Yang,Yue Yang,Guangchen Zu,Xianjun Yu,Weibo Chen,Yi Qin,Xiaowu Xu,Xuemin Chen
出处
期刊:Acta Biochimica et Biophysica Sinica [Oxford University Press]
标识
DOI:10.3724/abbs.2024153
摘要

Pancreatic ductal adenocarcinoma (PDAC) is a highly malignant disease with a poor prognosis, and the lack of effective treatment methods accounts for its high mortality. Pancreatic stellate cells (PSCs) in the tumor microenvironment play an important role in the development of PDAC. Previous studies have reported that patients with PDAC are more vulnerable to ferroptosis inducers. To investigate the relationship between PSCs and pancreatic cancer cells, a coculture system is used to further reveal the influence of PSCs on ferroptosis resistance in PDAC using many in vitro and in vivo experiments. Our results show that PSCs promote ferroptosis resistance in pancreatic cancer cells. We further demonstrate that IL15 secretion by PSCs activates the IL15RA-STAT3-GPX4/ACSL3 axis. The simultaneous upregulation of GPX4 and ACSL3 prevents lipid peroxidation and ultimately protects pancreatic cancer cells from ferroptosis both in vitro and in vivo. This study demonstrates that PSCs protect pancreatic cancer cells in a paracrine manner and may indicate a novel strategy for the treatment of PDAC.

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