GLUT3 drives paclitaxel resistance in peritoneal metastatic gastric cancer by promoting H3K18 lactylation-mediated MAPKAP1 transcription to suppress ferroptosis

International Journal of Biological Sciences 2026 Open access

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Authors: Ying Sun, Xirui Duan, Benyan Zhang, Cheng Xiong, Jun Ji, Qu Cai, Wang Yao, Jinling Jiang, Junwei Wu, Chao Wang, Liting Guo, Chenfei Zhou
+3 more Beiqin Yu, Qi Feng, Jun Zhang
DOI: 10.7150/ijbs.130059
Cited by: 1

Abstract

Background: Paclitaxel-based intraperitoneal chemotherapy (IPC) is a cornerstone strategy for treating gastric cancer peritoneal metastasis (GCPM). However, a subset of patients exhibit resistance to this therapy. Our study revealed that glucose transporter type 3 (GLUT3) is a key mediator of paclitaxel resistance in GCPM, although its precise mechanism of action remains to be fully elucidated. Methods: ) but also significantly suppressed the expression of MAPKAP1, GPX4, and SLC7A11. Conclusion: Targeting GLUT3-H3K18la-MAPKAP1 reverses paclitaxel resistance by inducing ferroptosis, providing a novel combination strategy for treating refractory GCPM.

Fields of Study & Subjects

Ferroptosis and cancer prognosis Cancer Hypoxia and Metabolism Lipids

Publication details

Journal / source
International Journal of Biological Sciences
Publisher
Ivyspring International Publisher
Volume
22
Issue
9
Pages
4826–4846
Publication date
23 April 2026
Language
EN