miR-625 suppresses cell proliferation and migration by targeting HMGA1 in breast cancer

Biochem Biophys Res Commun. 2016 Feb 19;470(4):838-44. doi: 10.1016/j.bbrc.2016.01.122. Epub 2016 Jan 22.


Dysregulation of microRNA contributes to the high incidence and mortality of breast cancer. Here, we show that miR-625 was frequently down-regulated in breast cancer. Decrease of miR-625 was closely associated with estrogen receptor (P = 0.004), human epidermal growth factor receptor 2 (P = 0.003) and clinical stage (P = 0.001). Kaplan-Meier and multivariate analyses indicated miR-625 as an independent factor for unfavorable prognosis (hazard ratio = 2.654, 95% confident interval: 1.300-5.382, P = 0.007). Re-expression of miR-625 impeded, whereas knockdown of miR-625 enhanced cell viabilities and migration abilities in breast cancer cells. HMGA1 was confirmed as a direct target of miR-625. The expressions of HMGA1 mRNA and protein were induced by miR-625 mimics, but reduced by miR-625 inhibitor. Re-introduction of HMGA1 in cells expressing miR-625 distinctly abrogated miR-625-mediated inhibition of cell growth. Taken together, our data demonstrate that miR-625 suppresses cell proliferation and migration by targeting HMGA1 and suggest miR-625 as a promising prognostic biomarker and a potential therapeutic target for breast cancer.

Keywords: Breast cancer; HMGA1; Migration; Proliferation; miR-625.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Biomarkers, Tumor / metabolism*
  • Breast Neoplasms / metabolism*
  • Breast Neoplasms / mortality*
  • Breast Neoplasms / pathology
  • Cell Movement
  • Cell Proliferation
  • China / epidemiology
  • Female
  • HMGA1a Protein / metabolism*
  • Humans
  • Incidence
  • MicroRNAs / metabolism*
  • Middle Aged
  • Risk Factors
  • Survival Rate
  • Tumor Cells, Cultured
  • Young Adult


  • Biomarkers, Tumor
  • MIRN625 microRNA, human
  • MicroRNAs
  • HMGA1a Protein