In the present study, we observed that loss of RhoA function through RhoA-T19N largely mimicked miR-122-induced MET, and the inhibition of migration and invasion of tumor cells, whereas RhoA over-expression in miR-122-expressing Bel-7402 cells reversed miR-122-induced MET and abrogated the miR-122-mediated suppression of motility and invasion of HCC cells. Here, MET is linked to neoplasm.