Anti-RTKN2 monoclonal antibody

Hepatocellular carcinoma (HCC), which is one of the most common types of cancer worldwide, has been ranked as the third leading cause of cancer-associated mortality worldwide. Rhotekin 2 (RTKN2), a Rho-guanosine triphosphatase (GTPase) effector, has been reported to be anti-apoptotic. 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 BEL-7404 by RNA interference led to marked inhibition of cell proliferation and cell cycle progression. Notably, RTKN2 silencing significantly reduced the levels of cell cycle-associated proteins, proliferating cell nuclear antigen and cyclin-dependent 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.

Human osteosarcoma is the most frequent primary malignant of bone, and often occurs in adolescents. However, molecular mechanism of this disease remains unclear. In the present study, we found that the level of Rhotekin 2 (RTKN2) was up-regulated in osteosarcoma tissues and cell lines. In addition, silencing of RTKN2 of human osteosarcoma cell lines U2OS, inhibited proliferation, and induced G1 phase cell cycle arrest via reducing the level of the cyclin-dependent kinase 2 (CDK2). Furthermore, RTKN2 knockdown in the U2OS cells induced apoptosis by increasing the level of Bax and decreasing the level of Bcl2. These results suggested that RTKN2 is involved in the progression of human osteosarcoma, and may be a potential therapeutic target.