Abstract
Abstract Overexpressed CXC chemokine receptor (CXCR4) strongly contributes to breast cancer metastasis. However, the underlying mechanisms of CXCR4 overexpression need still to be explored. MicroRNAs (miRNA) have been implicated as a class of critical regulators controlling diverse biological processes. In the present study, we investigated whether miR-302 and miR-588 are involved in the regulation of CXCR4 and play a functional role in breast cancer metastasis. We have shown that miR-302 and miR-588 were downregulated in highly metastatic breast cancer cell lines and tissue specimens compared to low metastatic cell lines and breast cancer tissues. The decreased expression levels were inversely consistent with overexpression of CXCR4 in highly breast cancer cell lines and tissues. In addition, we found that restoration of miR-302 and miR-588 resulted in a dramatic reduction of CXCR4 expression at protein levels by directly targeting its 3′ untranslated region. Furthermore, the elevated expression of miR-302 and miR-588 significantly inhibited the invasion of breast cancer cells. More promisingly, our data have demonstrated that overexpression of miR-302 reduced metastasis and growth of breast cancer in vivo. Our findings describe a new mechanism for the regulation of CXCR4 and metastasis of breast cancer. The newly characterized miR-302/588/CXCR4 link provides potential molecular markers for predicting breast cancer metastasis. MiR-302 and miR-588 may have a therapeutic potential to suppress breast cancer metastasis. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2297. doi:1538-7445.AM2012-2297
Published Version
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