Silencing of NUF2 Inhibits Tumor Growth and Induces Apoptosis in Human Hepatocellular Carcinomas


Background: As an important component of the NDC80 kinetochore complex, NUF2 is essential forkinetochore-microtubule attachment and chromosome segregation. Previous studies also suggested its involvementin development of various kinds of human cancers, however, its expression and functions in human hepatocellularcarcinoma (HCC) are still unclear. Materials and
Methods: In the present study, we aimed to test the hypothesisthat NUF2 is aberrant in human HCCs and associated with cell growth.
Results: Our results showed significantlyelevated expression of NUF2 in human HCC tissues compared to adjacent normal tissues, and high expressionof NUF2 in HCC cell lines. Using lentivirus-mediated silencing of NUF2 in HepG2 human HCC cells, we foundthat NUF2 depletion markedly suppressed proliferation and colony formation capacity in vitro, and dramaticallyhampered tumor growth of xenografts in vivo. Moreover, NUF2 silencing could induce cell cycle arrest andtrigger cell apoptosis. Additionally, altered levels of cell cycle and apoptosis related proteins including cyclinB1, Cdc25A, Cdc2, Bad and Bax were also observed.
Conclusions: In conclusion, these results demonstrate thatNUF2 plays a critical role in the regulation of HCC cell proliferation and apoptosis, indicating that NUF2 mayserve as a potential molecular target for therapeutic approaches.