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片仔癀通过AKT-mTOR途径抑制卵巢癌细胞增殖。

Inhibition of ovarian cancer cell proliferation by Pien Tze Huang via the AKT-mTOR pathway.

作者信息

He Fan, Wu Hui-Ni, Cai Mu-Yan, Li Chang-Peng, Zhang Xin, Wan Quan, Tang Shuang-Bo, Cheng Jian-Ding

机构信息

Department of Forensic Medicine, Zhongshan Medical School, Sun Yat-Sen University, Guangzhou, Guangdong 510080, P.R. China.

Department of Preventive Medicine, School of Public Health, Sun Yat-Sen University, Guangzhou, Guangdong 510080, P.R. China.

出版信息

Oncol Lett. 2014 Jun;7(6):2047-2052. doi: 10.3892/ol.2014.1989. Epub 2014 Mar 21.

Abstract

Pien Tze Huang (PZH) is a well-known Chinese medicine that has been used as a therapeutic drug in the treatment of a number of diseases, such as hepatocellular carcinoma and colon cancer. However, few studies have analyzed the effects of PZH on ovarian cancer cell proliferation. In the present study, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and Transwell assays, cell cycle and apoptosis rate analyses and western blotting were conducted to investigate the effects of PZH on the proliferation rate of ovarian cancer cells and its potential molecular pathway. The results showed that PZH inhibits the proliferation of the human ovarian cancer OVCAR-3 cell line by blocking the progression of the cell cycle from the G to S phase, however, PZH did not induce OVCAR-3 cell apoptosis. Increased PZH concentration may downregulate the expression of AKT, phosphorylated (p)-AKT, mammalian target of rapamycin (mTOR) and p-mTOR proteins in the OVCAR-3 cell line. In addition, it was observed that PZH may suppress the protein expression of cyclin-dependent kinase (CDK)4 and CDK6. Overall, the results of the present study indicated that PZH may inhibit ovarian cancer cell proliferation by modulating the activity of the AKT-mTOR pathway.

摘要

片仔癀(PZH)是一种著名的中药,已被用作治疗多种疾病的药物,如肝细胞癌和结肠癌。然而,很少有研究分析片仔癀对卵巢癌细胞增殖的影响。在本研究中,进行了3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐和Transwell实验、细胞周期和凋亡率分析以及蛋白质印迹法,以研究片仔癀对卵巢癌细胞增殖率及其潜在分子途径的影响。结果表明,片仔癀通过阻断细胞周期从G期到S期的进程来抑制人卵巢癌OVCAR-3细胞系的增殖,然而,片仔癀并未诱导OVCAR-3细胞凋亡。片仔癀浓度的增加可能会下调OVCAR-3细胞系中AKT、磷酸化(p)-AKT、雷帕霉素靶蛋白(mTOR)和p-mTOR蛋白的表达。此外,观察到片仔癀可能会抑制细胞周期蛋白依赖性激酶(CDK)4和CDK6的蛋白表达。总体而言,本研究结果表明,片仔癀可能通过调节AKT-mTOR途径的活性来抑制卵巢癌细胞增殖。

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