[No authors listed]
Hepatocellular carcinoma (HCC), which is one of the most common types of cancer worldwide, has been ranked as the third leading cause of cancerâassociated mortality worldwide. Rhotekin 2 (RTKN2), a Rhoâguanosine triphosphatase (GTPase) effector, has been reported to be antiâapoptotic. However, the molecular mechanism underlying the biological function of RTKN2 in HCC is poorly defined. The current study reported that RTKN2 was overexpressed in 83% of HCC specimens compared with adjacent noncancerous tissues (n=30). Depletion of RTKN2 in HCC cells, HepG2 and BELâ7404 by RNA interference led to marked inhibition of cell proliferation and cell cycle progression. Notably, RTKN2 silencing significantly reduced the levels of cell cycleâassociated proteins, proliferating cell nuclear antigen and cyclinâdependent kinase 1. Additionally, it was identified that downregulation of RTKN2 in HCC cells notably induced cell apoptosis, while significantly repressing cell invasion. These data suggest that RTKN2 may act as an oncogene and inhibition of RTKN2 may be part of a novel therapeutic strategy for targeted HCC therapy.
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