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Cancer Research 68, 5004, July 1, 2008. doi: 10.1158/0008-5472.CAN-08-0180
© 2008 American Association for Cancer Research

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Priority Reports

miR-206 Expression Is Down-regulated in Estrogen Receptor {alpha}–Positive Human Breast Cancer

Naoto Kondo, Tatsuya Toyama, Hiroshi Sugiura, Yoshitaka Fujii and Hiroko Yamashita

Oncology, Immunology, and Surgery, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan

Requests for reprints: Hiroko Yamashita, Oncology, Immunology and Surgery, Nagoya City University Graduate School of Medical Sciences, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya 467-8601, Japan. Phone: 1-81-52-853-8231; Fax: 1-81-52-853-6440; E-mail: hirokoy{at}med.nagoya-cu.ac.jp.

Key Words: breast cancer • estrogen receptor {alpha} • microRNA • miR-206

Expression levels of estrogen receptor (ER) {alpha} 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 ERβ 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. [Cancer Res 2008;68(13):5004–8]




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 2008 by the American Association for Cancer Research.