Exploring the Mechanism of MTAP Regulation in Renal Cell Carcinoma
Posted: Wednesday, November 28, 2018
To further explore the mechanisms of methylthioadenosine phosphorylase (MTAP) on tumor suppression and regulation of renal cell carcinoma progression, Ching-Hsien Chen, PhD, of the University of California, Davis, and colleagues presented their genetic study findings at the American Society of Nephrology Kidney Week 2018 (Abstract FR-PO1033). They found that insulin growth factor 1 receptor (IGF-1R) appears to be a “driver pathway conferring [the] aggressive nature to MTAP-deleted kidney cancer.”
Immunohistochemistry and tissue microarray confirmed an inverse association between IGF-1R phosphorylation and MTAP expression; and Western blots showed an elevation of IGF-1R phosphorylation and signaling after MTAP knockout. Further testing was performed with an inhibitor of IFG-1R, linsitinib; after this treatment, a decrease in cell viability, migration, invasion, and colony-forming capabilities was noted by researchers.
This understanding of the relationship between MTAP-gene expression and IGF-1R signaling may help to further direct treatment in these types of renal cell carcinoma.