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Marsdenia tenacissima extract induces G_0/G_1 cell cycle arrest in human esophageal carcinoma cells by inhibiting mitogen-activated protein kinase(MAPK) signaling pathway

查看全文 作  者:FAN [1]Wei;SUN [1]Li;ZHOU Jing-[2]Qian;ZHANG [3]Cang;QIN [3]Song;TANG [3]Ying;LIU [3]Yang;LIN Sen-[4]Sen;YUAN Sheng-[1]Tao 高影响力作者 机构地区:[1]Jiangsu Center for Drug Screening, China Pharmaceutical University;[2]Department of Complex Prescription of Traditional Chinese Medicine, School of Chinese Material Medicine, China Pharmaceutical University;[3]Nanjing Sanhome Pharmaceutical Co., Ltd.;[4]Jiangsu Center for Pharmacodynamics Research and Evaluation, China Pharmaceutical University高影响力机构 出  处:《Chinese Journal of Natural Medicines》索引2015年第13卷第6期,共10页高影响力期刊 基  金:financially supported by National Natural Science Foundation of China(Nos.81302794,81071841,81102853);the Study of Marsdenia tenacissima extract(MTE):Study on quality control of antitumor traditional Chinese medicine Xiao-Ai-Ping injection(No.2011ZX09201-201) 摘  要:Marsdenia tenacissima extract(MTE, trade name: Xiao-Ai-Ping injection) is an extract of a single Chinese plant medicine. It has been used for the treatment of cancer in China for decades, especially for esophageal cancer and other cancers in the digestive tract. In the present study, the potential mechanism for MTE's activity in esophageal cancer was explored. The effects of MTE on the proliferation of human esophageal cancer cells(KYSE150 and Eca-109) were investigated by the MTT assay, the Brd U(bromodeoxyuridine) incorporation immunofluorescence assay, and flow cytometric analysis. MTE inhibited cell proliferation through inducing G0/G1 cell cycle arrest in KYSE150 and Eca-109. Western blot analysis was employed to determine protein levels in the MTE treated cells. Compared with the control cells, the expression levels of the cell cycle regulatory proteins cyclin D1/D2/D3, cyclin E1, CDK2/4/6(CDK: cyclin dependent kinase), and p-Rb were decreased significantly in the cells treated with MTE at 40 mg·m L-1. In addition, MTE had an inhibitory effect on the MAPK(mitogen-activated protein kinase) signal transduction pathway, including ERK(extracellular signal-regulated kinase), JNK(c-Jun N-terminal kinase), and p38 MAPK. Moreover, MTE showed little additional effects on the regulation of cyclin D1/D3, CDK4/6, and p-Rb when the ERK pathway was already inhibited by the specific ERK inhibitor U0126. In conclusion, these data suggest that MTE inhibits human esophageal cancer cell proliferation through regulation of cell cycle regulatory proteins and the MAPK signaling pathways, which is probably mediated by the inhibition of ERK activation. 关 键 词:Marsdenia tenacissima extract Cell cycle arrest Mitogen-activated protein kinase signaling pathway Human esophageal cancer
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