KMT2D deficiency confers a therapeutic vulnerability to glycolytic and IGFR inhibitors in melanoma.
We reported that histone H3 lysine (K) 4 methyltransferase, KMT2D, serves as a potent tumor-suppressor in melanoma, which was identified via in vivo epigenome-focused RNA interference (RNAi) screen. KMT2D-deficient tumors show substantial reprogramming of key metabolic pathways including glycolysis via reduction of H3K4me1 (Histone H3K4 mono-methylation)-marked active enhancers, conferring sensitivity to inhibitors of glycolysis and IGFR (Insulin Growth Factor Receptor) pathway.
['Murugesan|Navya|N|https://orcid.org/0000-0001-9654-9783', 'Maitituoheti|Mayinuer|M|https://orcid.org/0000-0001-7185-997X']
KMT2D melanoma glycolysis enhancer reprogramming