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    Title: Akt inhibitor SC66 promotes cell sensitivity to cisplatin in chemoresistant ovarian cancer cells through inhibition of COL11A1 expression
    Authors: Wu, Yi-Hui
    Huang, Yu-Fang
    Chien-Chin Chen(陳建欽)
    Chou, Cheng-Yang
    Contributors: Natl Cheng Kung Univ, Coll Med, Natl Cheng Kung Univ Hosp, Dept Obstet & Gynecol
    Chia Yi Christian Hosp, Depardnent Pathol
    Chia Nan Univ Pharm & Sci, Dept Cosmet Sci
    Date: 2019-04
    Issue Date: 2020-07-29 13:55:16 (UTC+8)
    Abstract: We studied Akt inhibition using SC66 in a NOD-SCID xenograft mouse model and a panel of eight ovarian cancer cell lines. Elevated phospho-Akt levels in cancerous tissue were associated with short progression-free survival and overall survival. Cell sensitivity to SC66 was inversely correlated with phospho-Akt and COL11A1 expression levels, as well as resistance to cisplatin or paclitaxel. SC66 inhibited phosphorylation of Akt and its downstream effectors 4EBP1 and p70S6 kinase. SC66 also attenuated expression of TWIST1 and Mcl-1, factors important in cell invasiveness and antiapoptosis, respectively. SC66-sensitized chemoresistant cells to cisplatin and paclitaxel treatment, and promoted apoptosis. In addition, SC66 inhibited COL11A1 expression via decreased binding of CCAAT/enhancer-binding protein beta (c/EBP beta), reducing chemoresistance and decreasing binding of nuclear transcription factor Y (NF-YA) to COL11A1. A mouse xenograft experiment demonstrated that SC66 treatment caused a reduction in tumor formation and enhanced the therapeutic efficacy of cisplatin. This study demonstrates the role of Akt in ovarian tumor progression and chemoresistance, and supports the application of SC66 as a therapy for ovarian cancer.
    Relation: Cell Death & Disease, v.10, 322
    Appears in Collections:[Dept. of Cosmetic Science and institute of cosmetic science] Periodical Articles

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