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远志多糖PTP通过线粒体途径诱导卵巢癌细胞凋亡。

Polygala tenuifolia polysaccharide PTP induced apoptosis in ovarian cancer cells via a mitochondrial pathway.

作者信息

Zhang Fubin, Song Xiaowei, Li Li, Wang Jingfang, Lin Leyuan, Li Cong, Li Hongtao, Lv Yanju, Jin Yinghua, Liu Ying, Hu Yu, Xin Tao

机构信息

Department of Gynecology, The Third Affiliated (Tumor) Hospital, Harbin Medical University, Harbin, 150040, China.

出版信息

Tumour Biol. 2015 Apr;36(4):2913-9. doi: 10.1007/s13277-014-2921-x. Epub 2014 Dec 12.

DOI:10.1007/s13277-014-2921-x
PMID:25501282
Abstract

One purified polysaccharide protein tyrosine phosphatase (PTP) was isolated from the roots of Polygala tenuifolia. The aim of the present study is to investigate the antitumor effect of PTP on human ovarian cancer OVCAR-3 cells and explore the molecular mechanism of the action involved. The results of MTT assay and apoptosis detection assay showed that PTP inhibited cellular proliferation of OVCAR-3 cells and induced apoptotic cellular death via arresting cell circle at the G0/G1 phase. Reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analysis identified that bcl-2 gradually decreased at both transcription and protein levels after PTP treatment for 48 h in OVCAR-3 cells, while those of bax, cytochrome c, caspase-3, and caspase-9 increased. In addition, the low expression of NF-κB in PTP-treated OVCAR-3 cells would trigger the extrinsic pathway of programmed cell death signaling in tumor cells. These results together suggest that PTP may induce apoptosis of OVCAR-3 cells through a mitochondrial pathway.

摘要

从远志根中分离出一种纯化的多糖蛋白酪氨酸磷酸酶(PTP)。本研究旨在探讨PTP对人卵巢癌OVCAR-3细胞的抗肿瘤作用,并探索其作用的分子机制。MTT法和凋亡检测试验结果表明,PTP抑制OVCAR-3细胞的细胞增殖,并通过将细胞周期阻滞在G0/G1期诱导细胞凋亡死亡。逆转录-聚合酶链反应(RT-PCR)和蛋白质免疫印迹分析表明,在OVCAR-3细胞中用PTP处理48小时后,bcl-2在转录和蛋白质水平上逐渐降低,而bax、细胞色素c、半胱天冬酶-3和半胱天冬酶-9的水平升高。此外,PTP处理的OVCAR-3细胞中NF-κB的低表达会触发肿瘤细胞程序性细胞死亡信号的外源性途径。这些结果共同表明,PTP可能通过线粒体途径诱导OVCAR-3细胞凋亡。

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