Intracellular galectin-3 is a lipopolysaccharide sensor that promotes glycolysis through mTORC1 activation

Xing Chen, Chunyu Yu, Xinhua Liu, Beibei Liu, Xiaodi Wu, Jiajing Wu, Dong Yan, Lulu Han, Zifan Tang, Xinyi Yuan, Jianqiu Wang, Yue Wang, Shumeng Liu, Lin Shan and Yongfeng Shang ()
Additional contact information
Xing Chen: Capital Medical University
Chunyu Yu: Hangzhou Normal University
Xinhua Liu: Hangzhou Normal University
Beibei Liu: Capital Medical University
Xiaodi Wu: Capital Medical University
Jiajing Wu: Capital Medical University
Dong Yan: Capital Medical University
Lulu Han: Capital Medical University
Zifan Tang: Capital Medical University
Xinyi Yuan: Hangzhou Normal University
Jianqiu Wang: Hangzhou Normal University
Yue Wang: Hangzhou Normal University
Shumeng Liu: Capital Medical University
Lin Shan: Capital Medical University
Yongfeng Shang: Capital Medical University

Nature Communications, 2022, vol. 13, issue 1, 1-18

Abstract: Abstract How the carbohydrate binding protein galectin-3 might act as a diabetogenic and tumorogenic factor remains to be investigated. Here we report that intracellular galectin-3 interacts with Rag GTPases and Ragulator on lysosomes. We show that galectin-3 senses lipopolysaccharide (LPS) to facilitate the interaction of Rag GTPases and Ragulator, leading to the activation of mTORC1. We find that the lipopolysaccharide/galectin-3-Rag GTPases/Ragulator-mTORC1 axis regulates a cohort of genes including GLUT1, and HK2, and PKM2 that are critically involved in glucose uptake and glycolysis. Indeed, galectin-3 deficiency severely compromises LPS-promoted glycolysis. Importantly, the expression of HK2 is significantly reduced in diabetes patients. In multiple types of cancer including hepatocellular carcinoma (HCC), galectin-3 is highly expressed, and its level of expression is positively correlated with that of HK2 and PKM2 and negatively correlated with the prognosis of HCC patients. Our study unravels that galectin-3 is a sensor of LPS, an important modulator of the mTORC1 signaling, and a critical regulator of glucose metabolism.

Date: 2022
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DOI: 10.1038/s41467-022-35334-x

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