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BMC Cancer 2012
miRNA-135a promotes breast cancer cell migration and invasion by targeting HOXA10Abstract: Expression levels of miR-135a in tissues and cells were determined by poly (A)-RT PCR. The effect of miR-135a on proliferation was evaluated by CCK8 assay, cell migration and invasion were evaluated by transwell migration and invasion assays, and target protein expression was determined by western blotting. GFP and luciferase reporter plasmids were constructed to confirm the action of miR-135a on downstream target genes including HOXA10. Results are reported as means ± S.D. and differences were tested for significance using 2-sided Student"s t-test.Here we report that miR-135a was highly expressed in metastatic breast tumors. We found that the expression of miR-135a was required for the migration and invasion of breast cancer cells, but not their proliferation. HOXA10, which encodes a transcription factor required for embryonic development and is a metastasis suppressor in breast cancer, was shown to be a direct target of miR-135a in breast cancer cells. Our analysis showed that miR-135a suppressed the expression of HOXA10 both at the mRNA and protein level, and its ability to promote cellular migration and invasion was partially reversed by overexpression of HOXA10.In summary, our results indicate that miR-135a is an onco-miRNA that can promote breast cancer cell migration and invasion. HOXA10 is a target gene for miR-135a in breast cancer cells and overexpression of HOXA10 can partially reverse the miR-135a invasive phenotype.Micro RNAs (miRNAs) are small non-coding, cellular RNAs (17-27 bp) that post-transcriptionally regulate gene expression by inducing the degradation or translational repression of target mRNAs. The discovery of miRNAs and their mode of action has revealed an entirely new level of gene regulation. miRNAs must be assembled into a complex termed the RNA induced silencing complex (RISC) in order to regulate expression of their mRNA targets. Once assembled they act by binding to the 3'untranslated region (3'-UTR) and inducing degradation or transcr
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