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.