MicroRNA‑466 inhibits cancer cell migration and invasion in hepatocellular carcinoma by indirectly mediating the downregulation of ROCK2
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- Published online on: June 25, 2019 https://doi.org/10.3892/etm.2019.7709
- Pages: 1493-1499
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Copyright: © Ai et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Abstract
MicroRNA‑466 was recently characterized as a tumor suppressor with known biological function in prostate cancer. The aim of the current study was to investigate the possible involvement of microRNA‑466 in hepatocellular carcinoma (HCC). The current study demonstrated that the expression level of microRNA‑466 was significantly downregulated; while the mRNA expression level of Rho‑associated coiled‑coil containing protein kinase 2 (ROCK2) was significantly upregulated in tumor tissue compared with adjacent healthy tissue samples obtained from patients with HCC. In addition, the relative plasma level of microRNA‑466 was significantly decreased, while the relative plasma level of ROCK2 was significantly increased in patients with HCC compared with healthy controls. Expression levels of microRNA‑466 and ROCK2 were inversely correlated in tumor tissue but not in adjacent healthy tissue samples obtained from patients with HCC. Plasma levels of microRNA‑466 and ROCK2 were inversely correlated in patients with HCC but not in healthy controls. In addition, reduced plasma levels of microRNA‑466 may have a diagnostic value in the detection of early stage HCC. MicroRNA‑466 overexpression significantly suppressed ROCK2 expression in HCC cells, whereas ROCK2 overexpression did not significantly affect microRNA‑466 expression. MicroRNA‑466 overexpression significantly suppressed, while ROCK2 overexpression significantly enhanced HCC cell migration and invasion. In addition, ROCK2 overexpression partially reversed the inhibitory effect of microRNA‑466 overexpression on HCC cell migration and invasion. Taken together, these results suggest that microRNA‑466 may inhibit HCC cell migration and invasion by indirectly mediating the downregulation of ROCK2.
