[Overexpression of estrogen receptor-related receptor alpha can stimulate estrogen receptor negative endometrial cancer cell proliferation]

Zhonghua Fu Chan Ke Za Zhi. 2007 Jun;42(6):408-11.
[Article in Chinese]

Abstract

Objective: To investigate the role of human estrogen receptor-related receptor (ERR) alpha, a submember of orphan receptors, in the tumorigenesis of endometrial cancer.

Methods: Plasmid of pSG-ERRalpha was transfected into endometrial cancer cell lines HEC-1A, HEC-1B, and Ishikawa. Real-time quantitative RT-PCR and western blot were used to analyze the mRNA and protein expression of ERRalpha in endometrial cancer cell. Flow cytometry was used to analyze the cellular growth.

Results: Expressions of the ERRalpha were significantly increased in the endometrial cancer cells transfected with pSG-ERRalpha plasmid; expression of the ERRalpha mRNA in HEC-1A cell was 9644.4 copies/ng, HEC-1B: 9835.3 copies/ng, and Ishikawa: 8008.6 copies/ng (P < 0.01); expression of the ERRalpha protein in HEC-1A cell was 1.128, HEC-1B: 1.104, and Ishikawa: 1.008 (P < 0.05). Flow cytometry showed over-expression of ERRalpha was accompanied by increased HEC-1A and HEC-1B cells in S and G(2)/M phase (P < 0.01), while this could not be observed in the estrogen receptor (ER) positive endometrial cancer cell line Ishikawa. Furthermore, cellular growth analysis showed that over-expression of ERRalpha induced cell growth increase of the ER negative endometrial cancer cells HEC-1A and HEC-1B (P < 0.05).

Conclusion: Over-expression of ERRalpha could stimulate ER negative endometrial cancer cell proliferation independent of estrogen-ER pathway.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Blotting, Western
  • Cell Cycle
  • Cell Line, Tumor
  • Cell Proliferation*
  • ERRalpha Estrogen-Related Receptor
  • Endometrial Neoplasms / genetics
  • Endometrial Neoplasms / metabolism
  • Endometrial Neoplasms / pathology
  • Female
  • Flow Cytometry
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Plasmids
  • RNA, Messenger / biosynthesis
  • RNA, Messenger / genetics
  • Receptors, Estrogen / biosynthesis
  • Receptors, Estrogen / genetics*
  • Receptors, Estrogen / physiology
  • Reverse Transcriptase Polymerase Chain Reaction
  • Transfection

Substances

  • RNA, Messenger
  • Receptors, Estrogen