Inhibition of RAD54B suppresses proliferation and promotes apoptosis in hepatoma cells.

Abstract

RAD54 homolog B is a central motor protein of homologous recombination (HR), which plays an important role in the development and evolution of human cancer. Recent studies have indicated that RAD54B is aberrantly expressed in a variety of cancers and exhibits numerous biological functions, including participating in the repair of DNA double strand breaks. However, the expression and function of RAD54B in liver cancer have not yet been reported. The aim of the present study was to investigate the expression of RAD54B and elucidate its role in liver cancer cell lines by inhibiting RAD54B using a lentivirus-mediated shRNA interference system. We also assessed the effect of RAD54B on cell proliferation, colony formation, cell cycle distribution and cell apoptosis in BEL-7404 and SMMC-7721 cell lines using shRAD54B or shCtrl transfection. Furthermore, we analyzed the relationship between the expression of RAD54B protein, as measured by immunohistochemical staining, and the prognosis of patients with hepatoma. We found that RAD54B was highly expressed in liver cancer cell lines compared with the normal hepatic cell line LO2. Similarly, positive expression of RAD54B, which is associated with poor prognosis, was also observed in 52/83 samples of liver cancer tissue. Additionally, RAD54B downregulation significantly inhibited cell proliferation and colony formation, while also inducing G1/S cell cycle arrest and apoptosis in BEL-7404 and SMMC-7721 cells. These results indicated that RAD54B has oncogenic properties, and may be a potential treatment target for liver cancer patients.