GLUT1 promotes cell proliferation via binds and stabilizes phosphorylated EGFR in lung adenocarcinoma

文献类型： 外文期刊

第一作者： Zhou, Zhiqing

作者： Zhou, Zhiqing;Li, Yu;Chen, Sijie;Xie, Zhangrong;Du, Yuhui;Liu, Yue;Shi, Yuxuan;Lin, Xiangyi;Zeng, Xiaofei;Zhao, Huijie;Chen, Guoan;Zeng, Xiaofei;Zhao, Huijie;Chen, Guoan

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关键词： LUAD; GLUT1; EGFR; Gefitinib; WZB117

期刊名称：CELL COMMUNICATION AND SIGNALING （ 影响因子：8.4； 五年影响因子：8.0 ）

ISSN：

年卷期： 2024 年 22 卷 1 期

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收录情况： SCI

摘要： Background While previous studies have primarily focused on Glucose transporter type 1 (GLUT1) related glucose metabolism signaling, we aim to discover if GLUT1 promotes tumor progression through a non-metabolic pathway.Methods The RNA-seq and microarray data were comprehensively analyzed to evaluate the significance of GLUT1 expression in lung adenocarcinoma (LUAD). The cell proliferation, colony formation, invasion, and migration were used to test GLUT1 's oncogenic function. Co-immunoprecipitation and mass spectrum (MS) were used to uncover potential GLUT1 interacting proteins. RNA-seq, DIA-MS, western blot, and qRT-PCR to probe the change of gene and cell signaling pathways.Results We found that GLUT1 is highly expressed in LUAD, and higher expression is related to poor patient survival. GLUT1 knockdown caused a decrease in cell proliferation, colony formation, migration, invasion, and induced apoptosis in LUAD cells. Mechanistically, GLUT1 directly interacted with phosphor-epidermal growth factor receptor (p-EGFR) and prevented EGFR protein degradation via ubiquitin-mediated proteolysis. The GLUT1 inhibitor WZB117 can increase the sensitivity of LUAD cells to EGFR-tyrosine kinase inhibitors (TKIs) Gefitinib.Conclusions GLUT1 expression is higher in LUAD and plays an oncogenic role in lung cancer progression. Combining GLUT1 inhibitors and EGFR-TKIs could be a potential therapeutic option for LUAD treatment.

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