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. 2015 Mar 30;6(15):13658–13670. doi: 10.18632/oncotarget.3700

Figure 3. MiR-200b subfamily negatively regulated RhoA and ROCK2 expression.

Figure 3

(a) and (b) Luciferase reporter assays. Wild-type and mutated RhoA or ROCK2 3′UTR were co-transfected with miR-200 precursors into BEL7402 cells. Overexpression of miR-200b and miR-200c significantly inhibited the luciferase activity associated with the wild-type 3′UTRs of RhoA and ROCK2. RLU: relative luciferase activity normalized with the empty miRNA luciferase reporter vector control. (c) and (d) qRT-PCR analysis showed that stable overexpression of miR-200b and miR-200c significantly inhibited endogenous RhoA and ROCK2 mRNA expression in BEL7402. (e) The endogenous RhoA and ROCK2 protein expression levels were reduced in miR-200b and miR-200c stably overexpressing cells. (f) Transient expression of miR-200 LNA inhibitors augmented endogenous RhoA and ROCK2 protein expression in immortalized hepatocyte cell line, MIHA. P-values were determined by t-test and compared to the corresponding vector control. *P < 0.05, **P < 0.01, ***P < 0.001.