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Oncol Rep. 2014 May;31(5):2085-92. doi: 10.3892/or.2014.3105. Epub 2014 Mar 21.

Suppressive role of miR-502-5p in breast cancer via downregulation of TRAF2.

Author information

1
Department of Pathology, First Affiliated Hospital and College of Basic Medical Science, China Medical University, Shenyang, Liaoning 110001, P.R. China.
2
Department of Pancreatic Surgery, First Affiliated Hospital, China Medical University, Shenyang, Liaoning 110001, P.R. China.
3
Department of Medical Genetics, China Medical University, Shenyang, Liaoning 110001, P.R. China.

Abstract

TRAF2 promotes cancer cell survival, proliferation and metastasis through the NF-κB pathway by directly interacting with various TNF recepors. However, the molecular mechanism of TRAF2 dysregulation in breast cancer remains to be elucidated. In the present study, miR-502-5p was predicted as a potential regulator of TRAF2. miR-502-5p was significantly downregulated in breast cancer tissues when compared to the level in paired normal breast tissues. The breast cancer cell lines including MCF-7 and MDA-MB-231 expressed a lower level of miR-502-5p when compared to the level in the non-malignant breast epithelial cell line MCF-10A. In vitro, miR-502-5p enhanced early apoptosis and inhibited proliferation of breast cancer cells. Luciferase reporter assay results showed that miR-502-5p could bind to the 3'-untranslated region of the TRAF2 gene, thus, exerting an inhibitory effect on TRAF2. Furthermore, silencing of TRAF2 exhibited effects similar to those of exogenous miR‑502-5p, while overexpression of TRAF2 partially abrogated miR-502-5p-mediated suppression in breast cancer cells. In conclusion, miR-502-5p may act as a tumor-suppressor gene by targeting oncogenic TRAF2 in breast cancer and, therefore, may be a potential diagnostic and anticancer therapeutic marker for breast cancer.

PMID:
24677135
DOI:
10.3892/or.2014.3105
[Indexed for MEDLINE]

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