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Cancer Gene Ther. 2014 Feb;21(2):60-7. doi: 10.1038/cgt.2013.82. Epub 2014 Jan 24.

Critical role of miR-10b in transforming growth factor-β1-induced epithelial-mesenchymal transition in breast cancer.

Author information

1
Department of Breast Disease Surgery, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.
2
Department of Oncology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.

Abstract

Epithelial-mesenchymal transition (EMT) is a key process in the tumor metastatic cascade that is characterized by the loss of cell-cell junctions and cell polarity, resulting in the acquisition of migratory and invasive properties. Recent evidence showed that altered microRNA-10b (miR-10b) expression was implicated in the occurrence of EMT of breast cancer. However, the exact role and underlying mechanisms of miR-10b in the EMT of breast cancer still remain unknown. In this study, miR-10b was found to be upregulated in breast cancer tissues and breast cancer cell lines and the expression of miR-10b was shown to be closely correlated with aggressiveness in breast cancer. Treating breast cancer cells with the miR-10b inhibitor increased E-cadherin expression while decreasing vimentin expression. At the same time, on inhibition of miR-10b, the invasion and proliferation ability of breast cancer cells also decreased. Transforming growth factor-β (TGF-β) is a multifunctional cytokine that induces EMT in multiple cell types. Here, we identified miR-10b as a target gene of TGF-β1. The expression of miR-10b increased during TGF-β1-induced EMT of breast cancer cells. Further study showed that inhibition of miR-10b expression partially reversed the EMT, invasion and proliferation induced by TGF-β1 in breast cancer cells. Taken together, these results demonstrated a novel function for miR-10b in TGF-β1-induced EMT in breast cancer and increased their metastatic potential. MiR-10b might become a possible target for gene therapy in breast cancer.

PMID:
24457988
DOI:
10.1038/cgt.2013.82
[Indexed for MEDLINE]

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