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Oncol Rep. 2014 Mar;31(3):1357-63. doi: 10.3892/or.2013.2934. Epub 2013 Dec 19.

miR-96 promotes tumor proliferation and invasion by targeting RECK in breast cancer.

Author information

1
Department of General Surgery, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, P.R. China.
2
Department of Microbiology and Genetic Institute, University of Paris 11, Paris, France.
3
Department of General Surgery, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200072, P.R. China.

Abstract

microRNAs (miRNAs) are small non-coding RNAs that post-transcriptionally regulate gene expression in diverse biological processes. The aim of the present study was to investigate the expression pattern of miR-96 in breast cancer and its biological role in tumor progression. The expression levels of miR-96 were analyzed in 38 breast cancer specimens and 6 breast cancer cell lines by quantitative reverse-transcription polymerase chain reaction (qRT-PCR). The effect of miR-96 on proliferation was evaluated by MTT assays, and cell migration and invasion were evaluated by transwell assays in MDA-MB-231 human breast cancer cells. Luciferase reporter assays were performed to validate the regulation of a putative target of miR-96. The effects of modulating miR-96 on endogenous levels of this potential target were subsequently confirmed via qRT-PCR and western blot analysis. We found that expression of miR-96 was commonly upregulated in breast cancer cells and breast cancer specimens when compared with that in non-malignant breast epithelial cells and adjacent normal tissues. Ectopic expression of miR-96 promoted cellular proliferation, migration and invasion of breast cancer cells, whereas inhibition of miR-96 suppressed those functions. Luciferase assays revealed that miR-96 directly bound to the 3'-untranslated region (3'-UTR) of RECK. qRT-PCR and western blot analysis confirmed that miR-96 regulated the expression of RECK both at the mRNA and protein levels. Knockdown of RECK expression in MDA-MB-231 cells by siRNA significantly promoted cell proliferation, migration and invasion. Collectively, miR-96 was significantly upregulated in breast cancer. our data also delineate the molecular pathway by which miR-96 promotes breast cancer proliferation, migration and invasion. Our findings may have important implications for the treatment of breast cancer.

PMID:
24366472
DOI:
10.3892/or.2013.2934
[Indexed for MEDLINE]

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