title: [Estradiol enhances the proliferation and migration of Ishikawa cells by promotion of angiogenesis induced by activation of NF-κB via AKT pathway].
abstract: OBJECTIVE
  The aim of this study was to explore whether estradiol induces the expression of VEGF and bFGF in the endometrial cancer Ishikawa cells by activation of NF-κB via AKT pathway, and its effect on cell proliferation.
  
  
  METHODS
  Western blot was used to detect the AKT protein expression in Ishikawa cells after stimulation with estradiol, and the effect of AKT inhibitor or ER inhibitor on the activation of AKT. TransAM kit was used to detect the NF-κB p65 activity. qPCR and Western blot were used to detect the expression of VEGF and bFGF mRNA and proteins in the Ishikawa cells after estradiol treatment (E2 group), and pretreated with AKT inhibitor (AKT group) or ER inhibitor (ER group) or NF-κB inhibitor (NF-κB group), following the estradiol treatment. Flow cytometry and CFSE (carboxyfluorescein diacetate, succinimidyl ester) staining were used to examine the cell proliferation. Transwell was used to detect the migration ability of Ishikawa cells.
  
  
  RESULTS
  Expression of p-AKT protein in the Ishikawa cells was markedly higher than that in the control group (P < 0.05). Expressions of p-AKT protein in the AKT and ER groups were significantly decreased than that in the E2 group (P < 0.05). The NF-κB activity was highest after stimulation with 1×10(-6) mol/L estradiol for 30 min to 1 h. AKT inhibitor significantly reduced the NF-κB activity (P < 0.05). The expressions of VEGF and bFGF mRNA and proteins in the E2 group were significantly increased than that in the control group (P < 0.05), and their expression in the AKT, ER and NF-κB groups were significantly decreased than that in the E2 group (P < 0.05). The proliferation and migration abilities of the Ishikawa cells were significantly increased after estradiol stimulation.
  
  
  CONCLUSIONS
  Estradiol induces the production of VEGF and bFGF through activating NF-κB via AKT pathway, and enhances the proliferation and migration ability of cancer cells.
authors.affiliation: Department of Gynecologic Oncology, Affiliated Hospital of Guangxi Medical University, Nanning 530021, China.
authors.forename: Honglin
authors.initials: H
authors.lastname: Song
authors.affiliation: Department of Gynecologic Oncology, Affiliated Hospital of Guangxi Medical University, Nanning 530021, China.
authors.forename: Shaofeng
authors.initials: S
authors.lastname: Liang
authors.affiliation: Department of Gynecologic Oncology, Affiliated Hospital of Guangxi Medical University, Nanning 530021, China. Email: zjq201008@hotmail.com.
authors.forename: Jieqing
authors.initials: J
authors.lastname: Zhang
authors.affiliation: Department of Gynecologic Oncology, Affiliated Hospital of Guangxi Medical University, Nanning 530021, China.
authors.forename: Li
authors.initials: L
authors.lastname: Li
mesh_terms: D045744:Cell Line, Tumor; D049109:Cell Proliferation; D016889:Endometrial Neoplasms; D004958:Estradiol / Q000378:metabolism*; D005260:Female; D006801:Humans; D016328:NF-kappa B / Q000378:metabolism*; D009389:Neovascularization, Pathologic / Q000378:metabolism*; D012333:RNA, Messenger; D015398:Signal Transduction
chemical_list: D016328:NF-kappa B; D012333:RNA, Messenger; D004958:Estradiol