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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/115458


    Title: Tannic acid attenuate AKT phosphorylation to inhibit UMUC3 bladder cancer cell proliferation
    Authors: Ming-Cheng, Cheng C;Chen, Ming-Cheng;Ann, Selvaraj;Rajula, Selvaraj Annseles;Ku, V Bharath;Kumar, V Bharath;Chiung-Hung;Hsu, Chiung-Hung;Hsua, Cecilia;Day, Cecilia Hsuan;Che, Ray-Jade;Chen, Ray-Jade;Wang, Tso-Fu;Wang, Tso-Fu;Padma, Vijaya;Viswanadha, Vijaya Padma;Li, Chi-Cheng;Li, Chi-Cheng;黃志揚;Huang, Chih-Yang
    Contributors: 醫學暨健康學院醫學檢驗暨生物技術學系
    Keywords: Apoptosis;BCL-XLl UMUC3;BCL2;Bladder cancer;Caspase;MCL-1;NANOG;SOX2;Tannic acid.
    Date: 2022-06-01
    Issue Date: 2023-03-29 02:24:12 (UTC+0)
    Publisher: 亞洲大學
    Abstract: Urothelial bladder cancer is rapidly spreading across Western countries, and therapy has shown little-to-moderate effects on bladder cancer. Thus, focusing on curbing cancer incidence has become crucial. The aim of the present study was to investigate the anticancer effects of Tannic acid (TA) in human bladder cancer. UMUC3 bladder cancer cells were treated with different concentrations of TA (0-100 ?M) and tested for cell viability, colony formation, and apoptosis. The involvement of the phosphoinositide-3 kinase (PI3K)/Akt pathway in the action of TA was examined. TA treatment significantly inhibited the viability and increased percentage of apoptotic cells, thereby decreasing antiapoptotic proteins (BCL2, MCL-1, and BCL-XL) expression, resulting in the Caspase-3 activation. TA treatment decreased stem cell markers expression such as SOX2, OCT4, and NANOG. Additionally, TA treatment significantly reduced the phosphorylation levels of Akt in bladder cancer cells. Our study demonstrates the growth inhibitory effects of TA in bladder cancer cells, and highlights its potential as an anticancer agent for bladder cancer.
    Appears in Collections:[Department of Biotechnology] Journal Article

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