| Background:Nuclear Auto-antigenic Sperm Protein (NASP), initially described as a highly auto-immunogenic testis and sperm-specific protein, is a histone chaperone that is proved to present in all dividing cells. NASP has two splice variants:tNASP and sNASP. Only cancer, germ, transformed, and embryonic cells have a high level of expression of the tNASP. Up to now, little has been known about tNASP in Renal cell carcinoma (RCC). In the present study, the molecular mechanism of tNASP in RCC was explored.Methods:The expression level of tNASP in16paired human RCC specimens was determined. Down-regulation of tNASP by siRNA was transfected in RCC cell lines. The effect of down-regulation of tNASP by siRNA on cell colony formation and proliferation was examined by colony formation assay and CCK-8assay; Cell cycle was analyzed by flow cytometry; The expression of cyclin D1and P21were detected by western bloting. ERK/MAPK signaling was also analyzed.Results:tNASP has a relative high expression level in human RCC tissues. Silence of tNASP inhibits proliferation induces cell cycle arrest by up-regulation of P21and down-regulation of cyclinD1. Furthermore, the regulating cell cycle-related proteins by silence of tNASP may be mediated by ERK signaling pathways.Conclusion:Our research demonstrates that knockdown of tNASP effectively inhibits the proliferation and causes G1phase arrest through ERK/MAPK signal pathway. |
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