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    Please use this identifier to cite or link to this item: http://ir.cnu.edu.tw/handle/310902800/31740


    標題: Protein disulfide isomerase a4 acts as a novel regulator of cancer growth through the procaspase pathway
    作者: Kuo, T-F
    Chen, T-Y
    Jiang, S-T
    Chen, K-W
    Chiang, Y-M
    Hsu, Y-J
    Liu, Y-J
    Chen, H-M
    Yokoyama, K. K.
    Tsai, K-C
    Yeh, H-H
    Chen, Y-R
    Yang, M-T
    Yang, C-Y
    Yang, W-C
    貢獻者: Acad Sinica, Agr Biotechnol Res Ctr
    Natl Taiwan Univ, Inst Biotechnol
    Natl Appl Res Labs, Natl Lab Anim Ctr
    Kaohsiung Med Univ, Grad Inst Med
    Natl Res Inst Chinese Med, Minist Hlth & Welf
    Taipei Med Univ, PhD Program Biotechnol Med
    Chia Nan Univ Pharm & Sci, Drug Discovery & Dev Ctr
    Natl Chung Hsing Univ, Grad Inst Biotechnol
    Acad Sinica, Taiwan Int Grad Program, Mol & Biol Agr Sci
    Natl Chung Hsing Univ
    Natl Chung Hsing Univ, Dept Life Sci
    Natl Yang Ming Univ, Inst Pharmacol
    Natl Taiwan Ocean Univ, Dept Aquaculture
    關鍵字: Endoplasmic-Reticulum Stress
    Induced Cell-Death
    Oxidoreductase Erp57
    Induced Apoptosis
    Inhibition
    Identification
    Generation
    Expression
    Viability
    Discovery
    日期: 2017-09-28
    上傳時間: 2018-11-30 15:54:55 (UTC+8)
    出版者: Nature Publishing Group
    摘要: Protein disulfide isomerase a4 (PDIA4) is implicated in the growth and death of tumor cells; however, its molecular mechanism and therapeutic potential in cancer are unclear. Here, we found that PDIA4 expression was upregulated in a variety of tumor cell lines and human lung adenocarcinoma tissues. Knockdown and overexpression of PDIA4 in tumor cells showed that PDIA4 facilitated cell growth via the reduction of caspases 3 and 7 activity. Consistently, Lewis lung carcinoma cells overexpressing PDIA4 grew faster than did parental cells in tumor-bearing mice, as shown by a reduced survival rate, increased tumor size and metastasis, and decreased cell death and caspases 3 and 7 activity. PDIA4 knockdown resulted in opposite outcomes. Moreover, results obtained in mice with spontaneous hepatoma indicated that PDIA4 deficiency significantly reduced hepatic tumorigenesis and cyst formation and increased mouse survival, tumor death, and caspases 3 and 7 activity. Mechanistic studies illustrated that PDIA4 negatively regulated tumor cell death by inhibiting degradation and activation of procaspases 3 and 7 via their mutual interaction in a CGHC-dependent manner. Finally, we found that 1,2-dihydroxytrideca-5,7,9,11-tetrayne, a PDIA4 inhibitor, reduced tumor development via enhancement of caspase-mediated cell death in TSA tumor-bearing mice. These findings characterize PDIA4 as a negative regulator of cancer cell apoptosis and suggest that PDIA4 is a potential therapeutic target for cancer.
    Appears in Collections:[藥學系(所)] 期刊論文

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