MiR-155 promotes gastric cancer growth and invasion by negatively regulating Transforming Growth Factor Beta Receptor 2

Summary

Gastric cancer (GC) has a high morbidity and mortality among the common malignancies worldwide. It is essential to elucidate the molecular events of GC proliferation and invasion, which will provide new therapeutic targets for GC. The inactivation of TGFβR2 is correlates with cancer cells growth and metastasis, but the mechanisms underlying the down-regulation of TGFβR2 expression remain unknown. MicroRNAs (miRNAs) act as post-transcriptional regulators play a key role in the development of cancers. The bioinformatics analysis and luciferase reporter assay demonstrated that miR-155 directly bind the 3′-untranslated region (3′-UTR) of TGFβR2 mRNA. In this study, we found that the TGFβR2 protein levels, but not mRNA levels, were down-regulated in GC tissues, while the levels of miR-155 were significantly increased in GC tissues. We deduced miR-155 inversely correlated with TGFβR2 in GC cells. In vitro studies showed that over-expression of miR-155 in SGC7901 inhibited the expression of TGFβR2 and then promoted GC cell proliferation and migration, whereas miR-155 inhibitor showed opposite effects. In addition, the tumor suppressing function of TGFβR2 was verified by using siRNA (small interfering RNA) and TGFβR2 over-expressing plasmid respectively. The results illustrated the miR-155 promotes cell growth and migration by negatively regulating TGFβR2. Thus, miR-155-regulated TGFβR2 as a potential therapeutic target in GC.

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