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    標題: Autophagy Drives Galectin-1 Secretion From Tumor-Associated Macrophages Facilitating Hepatocellular Carcinoma Progression
    作者: 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
    貢獻者: 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
    關鍵字: galectin-1
    hepatocellular carcinoma
    secretory autophagy
    tumor-associated macrophages
    toll-like receptor 2
    日期: 2021
    上傳時間: 2023-11-11 11:46:59 (UTC+8)
    出版者: FRONTIERS MEDIA SA
    摘要: 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>
    關聯: FRONT CELL DEV BIOL, v.9, pp.741820
    顯示於類別:[化妝品應用與管理系(所)] 期刊論文

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