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FOXO1 enhances G6PD expression to promote cancer cell antioxidative capacity 
Xianhong Zhang1,2 , Jie Zhang1,2 , Mengmeng Wei1,2 , Min Zhao1,2 , Xiaoxiong Wang3 , Yongfeng Hui3 , Dongdong Yuan1,2 , Zijiao Wang1,2 , Wei Wu1,2 , Peng Jiang4 , Yujiong Wang1,2,* , Le Li1,2,*
1School of Life Sciences, Ningxia University, Yinchuan 750021, China
2Key Laboratory of Ministry of Education for Protection and Utilization of Special Biological Resources in Western China, Ningxia University, Yinchuan 750021, China
3General Hospital of Ningxia Medical University, Yinchuan 750021, China
4School of Life Sciences, Tsinghua University, Beijing 100084, China
*Correspondence to:Le Li , Email:leli@nxu.edu.cn Yujiong Wang , Email:wyj@nxu.edu.cn
J Mol Cell Biol, Volume 17, Issue 5, May 2025, mjaf021,  https://doi.org/10.1093/jmcb/mjaf021
Keyword: FOXO1, G6PD, reactive oxygen species, survival, proliferation

Metabolic adaptability, controlled by transcription factors or oncogenes, is critical for the survival of cancer cells. However, the mechanism by which the transcription factor forkhead box protein O1 (FOXO1) regulates the proliferation and survival of malignant tumor cells under high levels of reactive oxygen species (ROS) remains poorly understood. Here, we found that FOXO1 endows cancer cells with the strong antioxidative capacity and rapid proliferation. By upregulating the expression of glucose-6-phosphate dehydrogenase (G6PD), the rate-limiting enzyme in the pentose phosphate pathway, FOXO1 promotes the synthesis of nicotinamide adenine dinucleotide phosphate and ribose 5-phosphate and thus enhances the antioxidative and proliferative capabilities of cancer cells. Induction of G6PD expression in FOXO1-deficient cells mitigates tumor growth inhibition and alleviates ROS level elevation. These results establish a critical role of FOXO1 in the regulation of G6PD during the antioxidative and proliferative processes of cancer cells.