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    Please use this identifier to cite or link to this item: https://ir.cnu.edu.tw/handle/310902800/34546

    標題: Protodioscin inhibits bladder cancer cell migration and growth, and promotes apoptosis through activating JNK and p38 signaling pathways
    作者: Chen, Yuan-Ru
    Wang, Shu-Chi
    Huang, Shu-Pin
    Su, Chia-Cheng
    Liu, Po-Len
    Cheng, Wei-Chung
    Chuu, Chih-Pin
    Chen, Jen-Kun
    Bao, Bo-Ying
    Lee, Cheng Hsueh
    Ke, Chien-Chih
    Wu, Hsin-En
    Chang, Hao-Han
    Yeh, Hsin-Chih
    Li, Chia-Yang
    貢獻者: Kaohsiung Medical University
    Kaohsiung Medical University Hospital
    Chi Mei Hospital
    Department of Senior Citizen Service Management, Chia Nan University of Pharmacy & Science
    China Medical University Taiwan
    Academia Sinica - Taiwan
    National Health Research Institutes - Taiwan
    Kaohsiung Municipal Ta-Tung Hospital
    關鍵字: methyl protodioscin
    日期: 2022
    上傳時間: 2023-12-11 13:57:11 (UTC+8)
    摘要: Bladder cancer is one of the most common malignancies of the male genitourinary urinary system. Protodioscin is a steroidal saponin with anti-cancer effects on several types of cancers; however, the anti-cancer activities of protodioscin on bladder cancer have not yet been investigated. Therefore, we aimed to examine the anti-cancer effects of protodioscin on bladder cancer. Two types of bladder cancer cell lines, non-muscle-invasive 5637 cells and muscle-invasive T24 cells, were used to evaluate the effects of protodioscin on cell growth, migration, invasion and epithelial-mesenchymal transition(EMT) marker expressions. Transcriptome analysis was performed by RNA-seq and validated using real-time PCR and western blot; additionally, an in vivo xenograft animal model was established and the anti-tumor effects of protodioscin were tested. Our results demonstrated that protodioscin inhibited cell proliferation, migration, motility and invasion on 5637 and T24 cells. Additionally, protodioscin also induced cell apoptosis and arrested the progression of cell cycle at G2 phase in bladder cancer cells. Moreover, protodioscin inhibited EMT through increased protein expression of E-cadherin and decreased protein expression of N-cadherin and vimentin. RNA-seq analysis indicated that protodioscin regulated mitogenactivated protein kinase(MAPK) and phosphoinositide 3-kinases(PI3K)/protein kinase B(AKT)/mammalian target of rapamycin(mTOR) signaling pathways as further verified by Western blot. Furthermore, protodioscin
    關聯: BIOMEDICINE & PHARMACOTHERAPY, v.156, December 2022, 113929
    Appears in Collections:[高齡福祉養生管理系] 期刊論文

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