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ER81-shRNA Inhibits Growth of Triple-negative Human Breast Cancer Cell Line MDA-MB-231 In Vivo and in Vitro

  • Chen, Yue (Department of Pathology, Kunming General Hospital) ;
  • Zou, Hong (Department of Pathology, Kunming General Hospital) ;
  • Yang, Li-Ying (Department of Pathology, Kunming General Hospital) ;
  • Li, Yuan (Department of Pathology, Kunming General Hospital) ;
  • Wang, Li (Department of Pathology, Kunming General Hospital) ;
  • Hao, Yan (Department of Pathology, Kunming General Hospital) ;
  • Yang, Ju-Lun (Department of Pathology, Kunming General Hospital)
  • Published : 2012.05.30

Abstract

The lack of effective treatment targets for triple-negative breast cancers make them unfitted for endocrine or HER2 targeted therapy, and their prognosis is poor. Transcription factor ER81, a downstream gene of the HER2, is highly expressed in breast cancer lines, breast atypical hyperplasia and primary breast cancers including triple-negative examples. However, whether and how ER81 affects breast cancer carcinogenesis have remained elusive. We here assessed influence on a triple-negative cell line. ER81-shRNA was employed to silence ER81 expression in the MDA-MB-231 cell line, and MTT, colony-forming assays, and flow cytometry were used to detect cell proliferation, colony-forming capability, cell cycle distribution, and cell apoptosis in vitro. MDA-MB-231 cells stably transfected with ER81-shRNA were inoculated into nude mice, and growth inhibition of the cells was observed in vivo. We found that ER81 mRNA and protein expression in MDA-MB-231 cells was noticeably reduced by ER81-shRNA, and that cell proliferation and clonality were decreased significantly. ER81-shRNA further increased cell apoptosis and the residence time in $G_0/G_1$ phase, while delaying tumor-formation and growth rate in nude mice. It is concluded that ER81 may play an important role in the progression of breast cancer and may be a potentially valuable target for therapy, especially for triple negative breast cancer.

Keywords

References

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