Autophagy Drives Galectin-1 Secretion From Tumor-Associated Macrophages Facilitating Hepatocellular Carcinoma Progression

doi:10.3389/fcell.2021.741820

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Title:	Autophagy Drives Galectin-1 Secretion From Tumor-Associated Macrophages Facilitating Hepatocellular Carcinoma Progression
Authors:	Davuluri, Goutham Venkata Naga Chen, Chien-Chin Chiu, Yen-Cheng Tsai, Hung-Wen Chiu, Hung-Chih Chen, Yuh-Ling Tsai, Pei-Jane Kuo, Wan-Ting Tsao, Nina Lin, Yee-Shin Chang, Chih-Peng
Contributors:	Natl Cheng Kung Univ, Coll Med, Inst Basic Med Sci Ditmanson Med Fdn Chia Yi Christian Hosp, Dept Pathol Chia Nan Univ Pharm & Sci, Dept Cosmet Sci Natl Cheng Kung Univ, Natl Cheng Kung Univ Hosp, Coll Med, Dept Internal Med,Div Gastroenterol & Hepatol Natl Cheng Kung Univ, Coll Med, Dept Pathol Natl Cheng Kung Univ, Coll Med, Inst Oral Med Natl Cheng Kung Univ, Dept Med Lab Sci & Biotechnol I Shou Univ, Coll Med, Dept Med Lab Sci Natl Cheng Kung Univ, Coll Med, Dept Microbiol & Immunol
Keywords:	galectin-1 hepatocellular carcinoma secretory autophagy tumor-associated macrophages toll-like receptor 2
Date:	2021
Issue Date:	2023-11-11 11:46:59 (UTC+8)
Publisher:	FRONTIERS MEDIA SA
Abstract:	Galectin-1 (Gal-1) is a secretory lectin with pro-tumor activities and is associated strongly with hepatocellular carcinoma (HCC) development. Although Gal-1 is a well-known soluble pro-tumor factor in the tumor microenvironment (TME), the secretion mode of Gal-1 is not clearly defined. On the other hand, in addition to cancer cells, Gal-1 is widely expressed in tumor stromal cells, including tumor-associated macrophages (TAMs). TAMs are a significant component of stromal cells in TME; however, their contributions in producing Gal-1 to TME are still not explored. Here we reveal that TAMs can actively secrete Gal-1 in response to stimuli of HCC cells. Gal-1 produced by TAMs leads to an increase of the systemic level of Gal-1 and HCC tumor growth in mice. Mechanistically, TLR2-dependent secretory autophagy is found to be responsible for Gal-1 secretion from TAMs. Gal-1 acts as a cargo of autophagosomes to fuse with multivesicular bodies via Rab11 and VAMP7-mediated vesicle trafficking before being secreted. This autophagy-regulated Gal-1 secretion in TAMs correlates to poor overall survival and progression-free survival rates of HCC patients. Our findings uncover the secretion mode of Gal-1 via secretory autophagy and highlight the pathological role of TAM-produced Gal-1 in HCC progression.</p>
Relation:	FRONT CELL DEV BIOL, v.9, pp.741820
Appears in Collections:	[Dept. of Cosmetic Science and institute of cosmetic science] Periodical Articles

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