MiR-181c modulates the proliferation, migration, and invasion of neuroblastoma cells by targeting Smad7

Yong Li, Hongwei Wang, Jianhua Li, and Wu Yue

The Fourth Clinical Hospital of Minimally Invasive Neurosurgery, Harbin Medical University, Harbin 150001, China

Acta Biochim Biophys Sin 2014, 46: 48–55; doi: 10.1093/abbs/gmt124

MicroRNAs (miRNAs) function as key regulators of gene expression in various cancers. In this study, the aim is to explore the roles and regulation mechanism of miR-181c in neuroblastoma (NB) cells. We found that miR-181c was downregulated in metastatic NB tissues, compared with primary NB tissues. Then functional studies indicated that miR-181c overexpression inhibited NB cell proliferation, migration, and invasion, while miR-181c inhibition increased cell proliferation, migration, and invasion. EGFP reporter assay, real-time polymerase chain reaction and western blot analysis validated that Smad7 was a direct target of miR-181c. MiR-181c reduced Smad7 expression at both mRNA and protein levels. Finally, functional assays showed that the effect of Smad7 knockdown on cells was similar to that of miR-181c overexpression. Importantly, Smad7 overexpression could restore the antitumor effects that were induced by miR-181c. In conclusion, our results demonstrated that miR-181c inhibits NB cell growth and metastasis-related traits through the suppression of Smad7, functioning as a tumor suppressor. Moreover, our results suggested that miR-181c may serve as an important therapeutic target for NB patients.

Prediction and validation targets for miR-181c

全文: http://abbs.oxfordjournals.org/content/46/1/48.full.pdf+html 

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