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. 2019 Dec 27;12:11507–11516. doi: 10.2147/OTT.S222564

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© 2019 Liu et al.

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ARHGAP10 negatively correlated with the active RhoA in CRC cells. (A, B). The level of active RHOA was downregulated in HT29 and RKO transfected with oeARHGAP10. **p < 0.01 vs oeNC. (C). The protein content of active RhoA was upregulated in siARHGAP10 transfected cells. ***p < 0.001 vs siNC. (D). The protein content of p-AKT was suppressed by the RhoA inhibitor CCG-1423 in siARHGAP10 transfected cells. **p < 0.01 vs siNC, ***p < 0.001 vs siNC; ^### p < 0.001 vs siARHGAP10. (E). The AKT agonist IGF-1 promoted the proliferation of siARHGAP10 transfected cells in the presence of RhoA inhibitor CCG-1423. **p < 0.01 vs siNC, ***p < 0.001 vs siNC; ^!!!p < 0.001 vs siARHGAP10; ^{^}p < 0.05 vs siNC+ CCG-1423, ^{^^^}p < 0.001 vs siNC+ CCG-1423; ^###p < 0.001 vs siARHGAP10 + CCG-1423. (F). The AKT agonist IGF-1 released the suppression of the RhoA inhibitor CCG-1423 in the metastasis of siARHGAP10 transfected cells. ***p < 0.001 vs siNC; ^!!!p < 0.001 vs siARHGAP10; ^{^^^}p < 0.001 vs siNC+ CCG-1423; ^###p < 0.001 vs siARHGAP10 + CCG-1423. (G). The protein contents of MMP2, MMP9 and p-AKT were promoted by the AKT agonist IGF-1 in siARHGAP10 transfected cells that cultured in the presence of RhoA inhibitor CCG-1423.