miR-342 is associated with estrogen receptor-α expression and response to tamoxifen in breast cancer

Estrogen receptor-alpha (ER alpha) is essential for estrogen-dependent growth and its level of expression is a crucial determinant of response to endocrine therapy and prognosis in ER alpha-positive breast cancer. Breast cancer patients show a wide range of ER alpha expression levels which change in individual patients during disease progression and in response to systemic therapies. However, little is known concerning how the expression of ER alpha is regulated in human breast cancer. Recently, several microRNAs (miRNAs) have been identified to regulate ER alpha expression and to predict ER, progesterone receptor (PR) and human epidermal growth factor 2 (HER2) status. The expression levels of miR-342 and ER alpha mRNA were analyzed in human breast cancer samples and cell lines by quantitative reverse transcription (RT)-PCR analysis. The correlations between the expression levels of miR-342 and clinicopathological factors were analyzed. Statistically significant associations were observed between miR-342 and ER, HER2 and vascular endothelial growth factor (VEGF) status in the human breast cancer samples and the levels of miR-342 gradually increased as ER alpha mRNA expression increased. Moreover, ectopic overexpression of miR-342 upregulated the expression levels of the ER alpha mRNA and significantly sensitized the MCF-7 cells to tamoxifen-induced apoptosis and inhibition of cellular proliferation. These results suggested that miR-342 expression is positively correlated with ER alpha mRNA expression in human breast cancer and that it may be a significant marker for predicting tamoxifen sensitivity in ERa-positive breast cancer and a potential target for restoring ERa expression and responding to antiestrogen therapy.