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MiR-630 suppresses non-small cell lung cancer by targeting vimentin

Objective: This study aimed to clarify the function of miR-630 on non-small cell lung cancer (NSCLC) cells.

Methods: Quantitative real-time PCR was utilized to detect the mRNA expression of miR-630 and vimentin (VIM) in NSCLC tissues and cells. The protein expression of VIM, P53, Caspase-3, Bcl-2, Bax and JAK2/STAT3 was evaluated via Western blot. Dual-luciferase reporter assay was applied to evaluate whether VIM is the target gene of miR-630. The migration, invasion, proliferation and apoptosis of NSCLC cells were examined by wound-healing assay, transwell assay, CCK-8 assay, and flow cytometry, respectively.

Results: MiR-630 was lowly expressed in NSCLC tissues and cells, while VIM was highly expressed in NSCLC cells. Dual-luciferase reporter assay data validated that miR-630 directly targeted VIM. MiR-630 overexpression inhibited VIM expression, but the inhibition of miR-630 upregulated VIM expression. Besides, miR-630 mimics restrained cell migration, invasion, and proliferation, and promoted NSCLC cell apoptosis. Whereas, VIM overexpression partly attenuated the inhibitory effect of miR-630 on NSCLC cells. Moreover, miR-630 mimics impeded p-JAK2 and p-STAT3 protein expression; and miR-630 inhibitor upregulated p-STAT3 and VIM protein expression, which was reversed after the addition of STAT3 inhibitor C188-9.

Conclusion: MiR-630 constrained the progression of NSCLC by inhibiting JAK2/STAT3 pathway and downregulating VIM expression.

Related Products

Cat.No. Product Name Information
S8605 C188-9 C188-9 (TTI 101) is a potent inhibitor of STAT3 that binds to STAT3 with high affinity (KD=4.7±0.4 nM). C188-9 is well tolerated in mice, shows good oral bioavailability, and is concentrated in tumors.

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