SKA2 promotes gastric cancer progression by regulating glutathione metabolism

iScience 2026 Open access

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Authors: Zhang Hai Peng, Jianfeng Zhong, Ting Zhou, Depei Jiang, Zijing Wang, Meifang Ye, Lekun Fang, Huizhen Xiong, He Chen
DOI: 10.1016/j.isci.2026.115202
Cited by: 0
References: 45

Abstract

. Mechanistically, SKA2 upregulates the glycine transporter SLC6A9, enhancing glycine uptake and glutathione (GSH) synthesis to maintain redox homeostasis. Consequently, SKA2 depletion disrupts this metabolic balance, leading to reactive oxygen species (ROS) accumulation and DNA damage. This oxidative stress activates the ATM/Chk2 pathway to trigger cell-cycle arrest and the ATM/JNK pathway to induce apoptosis. Our findings identify SKA2 as a critical driver of metabolic reprogramming that shields GC cells from oxidative stress-induced death, highlighting the SKA2-SLC6A9-GSH-ROS axis as a promising therapeutic target.

Fields of Study & Subjects

Redox biology and oxidative stress Sulfur Compounds in Biology Cancer Hypoxia and Metabolism

Publication details

Journal / source
iScience
Volume
29
Issue
4
Pages
115202–115202
Publication date
3 March 2026
Language
EN