miR-206 expression is down-regulated in estrogen receptor α-positive human breast cancer

Expression levels of estrogen receptor (ER) et govern estrogen-dependent growth, response to endocrine therapy, and prognosis in ER alpha-positive breast cancer. Multiple mechanisms involved in altering ER alpha gene expression in breast cancer have been identified, including ER alpha gene amplification as well as transcriptional silencing by DNA methylation of CpG islands within the ER alpha promoter and mutations within the open reading frame of ER alpha. However, expression levels of ER alpha in breast cancer tissues differ widely among patients, and frequently change during disease progression and in response to systemic therapies. Recent evidence has shown that microRNA mutations or misexpression correlate with various human cancers, and miR-206 is reported to decrease endogenous ER alpha mRNA and protein levels in human MCF-7 breast cancer cells via two specific target sites within the 3'-untranslated region of the human ER alpha transcript. In this study, we show for the first time that miR-206 expression is markedly decreased in ER alpha-positive human breast cancer tissues assayed by quantitative reverse transcription-PCR analysis. Moreover, we observe that miR-206 expression is inversely correlated with ER alpha but not ER,3 mRNA expression in breast cancer tissues. Transfection experiments revealed that introduction of miR-206 into estrogen-dependent MCF-7 breast cancer cells inhibits cell growth in a dose- and time-dependent manner. Our results suggest that miR-206 could be a novel candidate for endocrine therapy that targets only ER alpha in breast cancer.