Using CRISPR KO libraries in multiple isogenic melanoma cell lines with wildtype p16/ CDKN2A and p16/ CDKN2A knockdown, we determined that many nucleotide metabolism genes are negatively enriched in p16/ CDKN2A knockdown cells compared to controls. Whether other nucleotide metabolic genes and pathways are affected by p16/ CDKN2A loss and if these can be specifically targeted in p16-low tumors has not been previously explored. Interestingly, p16 also has roles in metabolic reprogramming, and we previously published that loss of p16 promotes nucleotide synthesis via the pentose phosphate pathway. In its canonical role, p16 inhibits the G1-S phase cell cycle progression through suppression of cyclin dependent kinases. P16 is a tumor suppressor encoded by the CDKN2A gene whose expression is lost in ~50% of all human cancers.
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