期刊
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
卷 44, 期 5, 页码 1785-1795出版社
Cell Physiol Biochem Press GmbH & Co
DOI: 10.1159/000485785
关键词
Mir-212-5p; Triple-negative breast cancer; Prrx2; Epithelial-to-mesenchymal transition
资金
- Natural Science Foundation of Shandong Province [ZR2017PH032]
- Higher Educational Science and Technology Program of Shandong Province [J17B092]
- National Natural Science Foundation of China [81302290, 81700029]
Background/Aims: Triple-negative breast cancer (TNBC) is the most aggressive breast cancer subtype. Our study investigated the functional role of miR-212-5p in TNBC. Methods: Realtime PCR was used to quantify miR-212-5p expression levels in 30 paired TNBC samples and adjacent normal tissues. Wound healing and Transwell assays were used to evaluate the effects of miR-212-5p expression on the invasiveness of TNBC cells. Luciferase reporter and Western blot assays were used to verify whether the mRNA encoding Prrx2 is a major target of miR-212-5p. Results: MiR-212-5p was downregulated in TNBC, and its expression levels were related to tumor size, lymph node status and vascular invasion in breast cancer. We also observed that the miR-212-5p expression level was significantly correlated with a better prognosis in TNBC. Ectopic expression of miR-212-5p induced upregulation of E-cadherin expression and downregulation of vimentin expression. The expression of miR212-5p also suppressed the migration and invasion capacity of mesenchymal-like cancer cells accompanied by a morphological shift towards the epithelial phenotype. Moreover, our study observed that miR-212-5p overexpression significantly suppressed Prrx2 by targeting its 3'-untranslated region (3'-UTR) region, and Prrx2 overexpression partially abrogated miR-212-5p-mediated suppression. Conclusions: Our study demonstrated that miR-212-5p inhibits TNBC from acquiring the EMT phenotype by downregulating Prrx2, thereby inhibiting cell migration and invasion during cancer progression. (c) 2017 The Author(s) Published by S. Karger AG, Basel
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