RbAp48 Is Critical for the Proliferation of Hypopharyngeal Carcinoma

Emerging evidence has indicated the significance of RbAp48 in tumorigenesis. Although many genetic and epigenetic factors have been found to be involved in the pathogenesis of hypopharyngeal carcinoma, the effect of RbAp48 in hypopharyngeal carcinoma is still unclear.

A stable cell line overexpressing RbAp48 was generated in FaDu cells. Cell proliferation and colony formation were detected using FaDu-RbAp48 cells. Next we utilized nude mouse xenografts to determine the role of RbAp48. Flow cytometry was employed to investigate the effect of RbAp48 in cell cycle distribution and apoptosis. Real-time PCR was used to detect the expression of tumor suppressors and apoptosis-related factors.

The overexpression of RbAp48 inhibited cell proliferation, colony formation, and tumor formation in nude mice. The overexpression of RbAp48 affected cell cycle distribution and induced apoptosis. The expression of p53, Rb, Bax, caspase 3, caspase 8, and caspase 9 was upregulated, whereas the expression of Bcl-2 was downregulated resulting from the overexpression of RbAp48.

RbAp48 was identified as critical in the proliferation of hypopharyngeal carcinoma in both in vitro and in vivo experiments. It is conceivable that the regulation of tumor suppressors (Bcl-2 family and caspase enzymes) by RbAp48 contributes, at least in part, to the RbAp48-mediated proliferation in hypopharyngeal carcinoma.