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

Friday, February 17, 2017
Exhibit Hall (Hynes Convention Center)
Andrew Fong, Bergen County Academies, Hackensack, NJ
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.