Molecular Biology Reports

, Volume 41, Issue 4, pp 1977–1984

MiR-200a is involved in proliferation and apoptosis in the human endometrial adenocarcinoma cell line HEC-1B by targeting the tumor suppressor PTEN

Authors

    • Laboratory of Reproductive BiologyChongqing Medical University
    • Department of Obstetrics and GynecologyThe First Affiliated Hospital of Chongqing Medical University
  • Jun-lin He
    • Laboratory of Reproductive BiologyChongqing Medical University
  • Xue-mei Chen
    • Laboratory of Reproductive BiologyChongqing Medical University
  • Chun-Lan Long
    • Pediatric Research Institute of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and DisordersChildren’s Hospital of Chongqing Medical University
  • De-Hui Yang
    • Laboratory of Reproductive BiologyChongqing Medical University
  • Yu-Bin Ding
    • Laboratory of Reproductive BiologyChongqing Medical University
    • Department of Obstetrics and GynecologyThe First Affiliated Hospital of Chongqing Medical University
  • Hong-Bo Qi
    • Department of Obstetrics and GynecologyThe First Affiliated Hospital of Chongqing Medical University
  • Xue-Qing Liu
    • Laboratory of Reproductive BiologyChongqing Medical University
Article

DOI: 10.1007/s11033-014-3045-5

Cite this article as:
Li, R., He, J., Chen, X. et al. Mol Biol Rep (2014) 41: 1977. doi:10.1007/s11033-014-3045-5

Abstract

Abnormal cell proliferation is a main driver of tumor formation and development, which involves the deletion, mutation, and downregulation of tumor suppressor genes. One study recently demonstrated that miR-200a plays an oncogenic role by inhibiting phosphatase and tensin homolog deleted on chromosome ten (PTEN) expression. In the human endometrial adenocarcinoma cell line HEC-1B, suppression of miR-200a expression inhibited cell proliferation and promoted apoptosis, whereas its over-expression had no effect on proliferation and apoptosis. Furthermore, inhibition or over-expression of miR-200a increased or reduced the expression of PTEN, respectively, with no change in PTEN mRNA levels. These effects were achieved by directly targeting miR-200a to the 3′ untranslated region of the PTEN mRNA to inhibit its translation. Taken together, we propose that in HEC-1B cells, miR-200a functions as an oncogene, affecting proliferation and apoptosis by regulating the expression of the tumor suppressor PTEN at the translational level.

Keywords

HEC-1B miR-200a PTEN Proliferation Apoptosis

Copyright information

© Springer Science+Business Media Dordrecht 2014