FBXO-25’s Viability of a Prognostic Indicator of Effective Cancer Treatment

Tumors occur when cells proliferate because of problems within a cell’s apoptotic processes. Colorectal adenocarcinoma, which accounts for 95% of all colon cancers, demonstrates an aberrant PRKCD-FBXO-25-HAX-1 axis where emerging research has shown that the PRKCD protein contributes to apoptosis, FBXO-25 is considered a tumor suppressor and, HAX-1 a proto-oncogene. The aberrant HAX-1 axis is anti-apoptotic, contributing to increased resistance to chemotherapeutic drugs. A study of the effect of FBXO-25 protein expression on HAX-1 activity is of interest in the treatment of this aggressive cancer, as HAX-1 has been suggested a substrate of FBXO-25. In the research reported, both cell viability and protein expression were measured through MTS assay and indirect ELISA in a colorectal adenocarcinoma cell line, HT29. Two groups of colorectal adenocarcinoma cells were used; one with FBXO-25 downregulated through interference RNA and another with constitutive FBXO-25 protein expression. FBXO-25’s effect on chemotherapeutic resistance was measured by treating both cell lines with varying concentrations of cisplatin ranging from 50µM – 3.125 µM for 24h. Downregulation of FBXO-25 rendered increased cellular viability (p<0.05) due to an increase in HAX-1 protein expression with increased chemotherapeutic resistance. With HAX-1 levels increased due to low FBXO-25 levels, this research suggests that levels of FBXO-25 can be used as a prognostic indicator in colorectal cancer.