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학술저널
저자정보
Ni, Jing (Department of Gynecologic Oncology, the Affiliated Cancer Hospital of Nanjing Medical University and Jiangsu Cancer Hospital) Wu, Qiang (Department of Gynecologic Oncology, the Affiliated Cancer Hospital of Nanjing Medical University and Jiangsu Cancer Hospital) Sun, Zhi-Hua (Department of Radiation of Gynecologic Oncology, the Affiliated Cancer Hospital of Nanjing Medical University and Jiangsu Cancer Hospital) Zhong, Jian (Department of Gynecologic Oncology, the Affiliated Cancer Hospital of Nanjing Medical University and Jiangsu Cancer Hospital) Cai, Yu (Department of Gynecologic Oncology, the Affiliated Cancer Hospital of Nanjing Medical University and Jiangsu Cancer Hospital) Huang, Xin-En (Department of Chemotherapy, the Affiliated Cancer Hospital of Nanjing Medical University and Jiangsu Cancer Hospital)
저널정보
아시아태평양암예방학회 Asian Pacific journal of cancer prevention : APJCP Asian Pacific journal of cancer prevention : APJCP 제16권 제11호
발행연도
2015.1
수록면
4,571 - 4,576 (6page)

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Background: To investigate the inhibitory effect and the underlying mechanism of triptolide on cultured human endometrial carcinoma HEC-1B cells and corresponding xenograft. Materials and Methods: For in vitro studies, the inhibition effect of proliferation on HEC-1B cell by triptolide was determined by MTT assay; cell cycle and apoptosis of the triptolide-treated and untreated cells were detected by flow cytometry. For in vivo studies, a xenograft tumor model of human endometrial carcinoma was established using HEC-1B cells, then the tumor-bearing mice were treated with high, medium, and low-dose ($8{\mu}g$, $4{\mu}g$ and $2{\mu}g/day$) triptolide or cisplatin at $40{\mu}g/day$ or normal saline as control. The mice were treated for 10-15 days, during which body weight of the mice and volume of the xenograft were weighted. Then expression of Bcl-2 and vascular endothelial growth factor (VEGF) was analyzed by SABC immunohistochemistry. Results: Cell growth was significantly inhibited by triptolide as observed by an inverted phase contrast microscope; the results of MTT assay indicated that triptolide inhibits HEC-1B cell proliferation in a dose and time-dependent manner; flow cytometry showed that low concentration (5 ng/ml) of triptolide induces cell cycle arrest of HEC-1B cells mainly at S phase, while higher concentration (40 or 80 ng/ml) induced cell cycle arrest of HEC-1B cells mainly at G2/M phase, and apoptosis of the cells was also induced. High-dose triptolide showed a similar tumor-inhibitory effect as cisplatin (-50%); high-dose triptolide significantly inhibited Bcl-2 and VEGF expression in the xenograft model compared to normal saline control (P<0.05). Conclusions: triptolide inhibits HEC-1B cell growth both in vitro and in mouse xenograft model. Cell cycle of the tumor cells was arrested at S and G2/M phase, and the mechanism may involve induction of tumor cell apoptosis and inhibition of tumor angiogenesis.

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