Targeting ROCK1/2 blocks cell division and induces mitotic catastrophe in hepatocellular carcinoma

Rho-Associated kinases ROCK1 and ROCK2 have been extensively investigated in the pathogenesis of cardiovascular disease. However, their roles are not fully understood carcinogenesis. In this study, we whether or is required for survival growth hepatocellular carcinoma (HCC) cells underlying mechanism. ROCKs expression was determined human HCC tissue cell lines using qRT-PCR, western blotting, immunohistochemistry (IHC). Cell proliferation were assayed counting kit-8 (CCK-8) EdU incorporation assay. cycle apoptosis analysis performed flow cytometry. division mitosis observed a confocal microscope time relapse fluorescence microscope. Inhibitory role targeting ROCK1/2 on both xenograft primary mouse models. Both over-expressed tissues lines. Knockdown inhibited growth. Pharmacological inactivation with Fasudil further blocked vitro vivo . Mechanically, induces arrest cells, but apoptosis. Instead, treatment led to mitotic catastrophe characterized multipolar asymmetric mitosis, disassociated stress fibers. cofilin restored morphology division, reduced induced by Fasudil. Targeting rather than can serve as potential approach may reduce side effects.