MicroRNA-195-5p is a potential diagnostic and therapeutic target for breast cancer

• DOI: 10.3892/or.2014.2971
• Publication Date: 2014-01-08T13:54:27Z
• Authors: QIFENG LUO; CHUANKUI WEI; XIAOYU LI; JIA LI; LEI CHEN; YIXIANG HUANG; HONGMING SONG; DENGFENG LI; LIN FANG
• Keywords: Oncogene Proteins; 0303 health sciences; Carcinoma, Ductal, Breast; Gene Expression; Breast Neoplasms; Articles; G1 Phase Cell Cycle Checkpoints; 3. Good health; Gene Expression Regulation, Neoplastic; MicroRNAs; 03 medical and health sciences; HEK293 Cells; Cell Movement; Cell Line, Tumor; Cyclin E; Biomarkers, Tumor; Humans; Female; RNA Interference; Cell Proliferation

MicroRNAs (miRNAs) are a class of highly conserved, small endogenous single-strand non-coding RNAs. They are aberrantly expressed in the circulation and tissue of patients with cancer. Therefore, it has been suggested that they may act as key regulators of carcinogenesis. The aim of the present study was to examine the expression level of miR-195-5p in human breast cancer and its potential role in carcinogenesis. The expression level of miR-195-5p was measured in 40 breast cancer specimens and adjacent normal breast tissues by quantitative polymerase chain reaction (qPCR). Next, to explore the potential function of miR-195-5p, we used MDA-MB-231 human breast cancer cells and carried out MTT, colony formation, Transwell chamber migration and cell cycle assays. The dual-luciferase reporter assay was also performed to determine putative targets of miR-195-5p, which were validated using qPCR and western blot assays. We found that miR-195-5p expression was significantly decreased in the 40 breast cancer specimens when compared with that in the adjacent normal breast tissues (P<0.05). Overexpression of miR-195-5p inhibited cell proliferation, reduced cell colony formation, suppressed cell migration and caused an accumulation of cells in the G1 phase of the cell cycle. In the 3'-untranslated region (3'-UTR) of cyclin E1 (CCNE1), we found two putative target sites which may bind miR-195-5p, suggesting that CCNE1 is a direct target of miR-195-5p. Furthermore, through qPCR and western blot assays we showed that overexpression of miR-195-5p reduced CCNE1 mRNA and protein levels, respectively. Our study suggests that miR-195-5p may act as a tumor suppressor in breast cancer. Therefore, targeting of this miRNA may provide a novel strategy for the diagnosis and treatment of patients with this lethal disease.