 RhoA mediates androgen-responsiveness of these SRF genes; as a result, interference with RhoA has been shown to prevent the androgen regulation of SRF genes.In application, RhoA expression is notably higher in malignant prostate cancer cells compared to benign prostate cells, with elevated RhoA expression being associated with elevated lethality and aggressive proliferation.On the other hand, silencing RhoA lessened androgen-regulated cell viability and handicapped prostate cancer cell migration.