Therefore, SNHG20 depletion could repress the in vivo tumor growth of OC through modulating miR-148a/ROCK1 axis. Therefore, according to the in vivo and in vitro results, a schematic figure (Fig. 7) was established to explain the role of up-regulation of SNHG20 enhanced ROCK1 expression by competitively binding miR-148a, which promoted OC cells EMT and proliferation was established to explain the role of up-regulation of SNHG20 enhanced ROCK1 expression by competitively binding miR-148a, which promoted OC cells EMT and proliferation. The gene discussed is ROCK1; the disease is neoplasm.