Mutations in the KRAS gene have long been known to cause cancer, and about one third of solid tumors have KRAS mutations or mutations in the KRAS pathway. KRAS promotes cancer formation not only by driving cell growth and division, but also by turning off protective tumor suppressor genes, which normally limit uncontrolled cell growth and cause damaged cells to self-destruct.
A new University of Iowa study provided a deeper understanding of how KRAS turns off tumor suppressor genes and identifies a key enzyme in the process. The findings, published online Nov. 26 in the journal Cell Reports, suggest that this enzyme, known as TET1, may be an important target for cancer diagnostics and treatment.
In KRAS-driven cancers, tumor suppressor genes are turned off, or silenced, because the DNA that controls their expression is modified by methylation. The UI study shows that KRAS promotes this methylation-associated gene silencing by turning off the TET1 enzyme, which can remove methyl marks from DNA.
