title: The Inhibition Effect of Triptolide on Human Endometrial Carcinoma Cell Line HEC-1B: a in vitro and in vivo Studies.
abstract: BACKGROUND
  To investigate the inhibitory effect and the underlying mechanism of triptolide on cultured human endometrial carcinoma HEC-1B cells and corresponding xenograft.
  
  
  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 μg, 4 μg and 2 μg/day) triptolide or cisplatin at 40 μg/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.
authors.affiliation: Department of Gynecologic Oncology, the Affiliated Cancer Hospital of Nanjing Medical University and Jiangsu Cancer Hospital, Nanjing, China E-mail : wqjsch@126.com, szhnj@163.com.
authors.forename: Jing
authors.initials: J
authors.lastname: Ni
authors.forename: Qiang
authors.initials: Q
authors.lastname: Wu
authors.forename: Zhi-Hua
authors.initials: ZH
authors.lastname: Sun
authors.forename: Jian
authors.initials: J
authors.lastname: Zhong
authors.forename: Yu
authors.initials: Y
authors.lastname: Cai
authors.forename: Xin-En
authors.initials: XE
authors.lastname: Huang
mesh_terms: D000818:Animals; D018906:Antineoplastic Agents, Alkylating / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D002453:Cell Cycle / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects*; D004224:Diterpenes / Q000494:pharmacology*; D016889:Endometrial Neoplasms / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology*; D004852:Epoxy Compounds / Q000494:pharmacology; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D066298:In Vitro Techniques; D051379:Mice; D010616:Phenanthrenes / Q000494:pharmacology*; D014407:Tumor Cells, Cultured; D023041:Xenograft Model Antitumor Assays
chemical_list: D018906:Antineoplastic Agents, Alkylating; D004224:Diterpenes; D004852:Epoxy Compounds; D010616:Phenanthrenes; C001899:triptolide