Back to Search
Start Over
miR-625 suppresses cell proliferation and migration by targeting HMGA1 in breast cancer.
- Source :
-
Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2016 Feb 19; Vol. 470 (4), pp. 838-44. Date of Electronic Publication: 2016 Jan 22. - Publication Year :
- 2016
-
Abstract
- 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.<br /> (Copyright © 2016 Elsevier Inc. All rights reserved.)
- Subjects :
- Adolescent
Adult
Aged
Breast Neoplasms pathology
Cell Movement
Cell Proliferation
China epidemiology
Female
Humans
Incidence
Middle Aged
Risk Factors
Survival Rate
Tumor Cells, Cultured
Young Adult
Biomarkers, Tumor metabolism
Breast Neoplasms metabolism
Breast Neoplasms mortality
HMGA1a Protein metabolism
MicroRNAs metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1090-2104
- Volume :
- 470
- Issue :
- 4
- Database :
- MEDLINE
- Journal :
- Biochemical and biophysical research communications
- Publication Type :
- Academic Journal
- Accession number :
- 26806308
- Full Text :
- https://doi.org/10.1016/j.bbrc.2016.01.122