Fig. 6: Proposed mechanism of correlation between TET1 expression, CGI methylation, and PRC2 regulation on tumor suppressors, including p16. | Cell Death & Disease

Fig. 6: Proposed mechanism of correlation between TET1 expression, CGI methylation, and PRC2 regulation on tumor suppressors, including p16.

From: Hypermethylation of CDKN2A CpG island drives resistance to PRC2 inhibitors in SWI/SNF loss-of-function tumors

Fig. 6

In normal cells, the function of PRC2 is regulated by the SWI/SNF complex, whereas in tumor cells featuring SWI/SNF LOF mutations in addition to TET1 expression, the recruitment of PRC2 on the p16 promoter is allowed to occur, and suppression of its expression by the H3K27me3 marker is mediated.

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