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    Please use this identifier to cite or link to this item: http://ir.cnu.edu.tw/handle/310902800/30900


    標題: Galectin-1-Induced Autophagy Facilitates Cisplatin Resistance of Hepatocellular Carcinoma
    作者: Su, Yu-Chi
    Davuluri, Goutham Venkata Naga
    Chen, Cheng-Hao
    Shiau, Dong-Che
    Chen, Chien-Chin
    Chen, Chia-Ling
    Lin, Yee-Shin
    Chang, Chih-Peng
    貢獻者: Natl Cheng Kung Univ, Coll Med, Dept Microbiol & Immunol
    Natl Cheng Kung Univ, Coll Med, Inst Basic Med Sci
    Chia Yi Christian Hosp, Dept Pathol
    Chia Nan Univ Pharm & Sci, Dept Cosmet Sci
    Taipei Med Univ, Translat Res Ctr
    Natl Cheng Kung Univ, Ctr Infect Dis & Signaling Res
    關鍵字: induced apoptosis
    ovarian-cancer
    cell-adhesion
    liver-cancer
    chemotherapy
    progression
    inhibition
    galectins
    differentiation
    chemoresistance
    日期: 2016-02
    上傳時間: 2018-01-18 11:37:33 (UTC+8)
    出版者: Public Library Science
    摘要: Hepatocellular carcinoma (HCC) is one of the most common cancers in Taiwan. Although chemotherapy is the primary treatment for HCC patients, drug resistance often leads to clinical failure. Galectin-1 is a beta-galactoside binding lectin which is up-regulated in HCC patients and promotes tumor growth by mediating cancer cell adhesion, migration and proliferation, but its role in chemoresistance of HCC is poorly understood. In this study we found that galectin-1 is able to lead to chemoresistance against cisplatin treatment, and subsequent inhibition has reversed the effect of cell death in HCC cells. Moreover, galectin-1 was found to induce autophagic flux in HCC cells. Inhibition of autophagy by inhibitors or knockdown of Atg5 cancels galectin-1-induced cisplatin resistance in HCC cells. Increase of mitophagy triggered by galectin-1 was found to reduce the mitochondrial potential loss and apoptosis induced by cisplatin treatment. Finally, using an in situ hepatoma mouse model, we clearly demonstrated that inhibition of galectin-1 by thiodigalactoside could significantly augment the anti-HCC effect of cisplatin. Taken together, our findings offer a new insight into the chemoresistance galectin-1 causes against cisplatin treatment, and points to a potential approach to improve the efficacy of cisplatin in the treatment of HCC patients.
    關聯: Plos One, v.11 n.2, e0148408
    Appears in Collections:[化妝品應用與管理系(所)] 期刊論文

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