Format

Send to

Choose Destination
Cell Physiol Biochem. 2014;34(6):2209-20. doi: 10.1159/000369664. Epub 2014 Dec 4.

MicroRNA-302b suppresses human epithelial ovarian cancer cell growth by targeting RUNX1.

Author information

1
Department of Gynecology, the Affiliated Tumor Hospital, Harbin Medical University, Harbin, China.

Abstract

BACKGROUND:

The microRNA (miR)-302 family functions as a tumor suppressor in human cancer. However, its role in epithelial ovarian carcinoma (EOC) remains unknown. Here, we investigated the role of miR-302b and its target gene RUNX1 in EOC.

METHODS:

The expression levels of miR-302b and RUNX1 were assessed by quantitative real-time PCR and western blotting. The effects of ectopic expression of miR-302b were evaluated by the MTT assay, colony forming assay and flow cytometry. RUNX1 was identified as a target of miR-302b and their interaction was confirmed by luciferase activity assays, RUNX1 silencing and overexpression of a RUNX1 mutant construct lacking the 3'UTR. The effect of miR-302b on the suppression of tumor growth was investigated in vivo in a xenograft mouse model.

RESULTS:

MiR-302b levels were markedly decreased in EOC specimens. Ectopic expression of miR-302b in EOC cells inhibited cell proliferation and colony formation, induced G0/G1 arrest, and promoted apoptosis. RUNX1 was identified as a direct target of miR-302b, and knockdown of RUNX1 inhibited cell growth in a manner similar to miR-302b overexpression, whereas introduction of a 3'UTR mutant of RUNX1 reversed the suppressive effect of miR-302b. Furthermore, miR-302b overexpression led to the inactivation of the STAT3 signaling pathway in EOC cells and inhibited tumor growth in a xenograft mouse model.

CONCLUSIONS:

MiR-302b functions as a tumor suppressor in EOC by targeting RUNX1 and modulating the activity of the STAT3 signaling pathway.

PMID:
25562167
DOI:
10.1159/000369664
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for S. Karger AG, Basel, Switzerland
Loading ...
Support Center