They found that RhoC, a Ras-related GTPase, is dispensable for embryonic development and tumor initiation, but is essential for metastasis. RhoC-deficient mice do not display gross phenotypical abnormalities or differences in the rate of induced tumorigenic potential, but RhoC-deficient mice do display markedly less tumor metastasis, compared to their wild-type littermates.
Preliminary results suggest that in RhoC deficient mice, the tumor cells have less motility (thus reduce the probability of cancer cells escaping from the primary tumors) as well as having reduced survival properties when they have spread to secondary sites and organs. Further research is underway to determine more clearly the mechanism of RhoC-induced metastasis.
The authors are confident that further investigation in to this pathway may help identify valuable targets for development of cancer therapeutics to prevent metastasis.