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Fig. 9 | Epigenetics & Chromatin

Fig. 9

From: MYC deregulates TET1 and TET2 expression to control global DNA (hydroxy)methylation and gene expression to maintain a neoplastic phenotype in T-ALL

Fig. 9

Working model: The MYC oncogene controls DNMT1 and DNMT3B, as well as TET1 and TET2 expression in T-ALL. Non-malignant cells: MYC levels are low, corresponding with low TET1, as well as DNMT1 and DNMT3B expression. Tumor cells: MYC levels are constitutively high, driving the expression of TET1 as well as DNMT1 and DNMT3B, while suppressing TET2. Regressing tumor: MYC inactivation in T-ALL causes tumor regression through cellular senescence. This is associated with diminished DNMT1, DNMT3B, and TET1 levels, while TET2 expression is increased. Loss of TET1 function (shRNA) and reconstitution of TET2 expression (cDNA) led to broad changes in 5mC and 5hmC patterns, in turn affecting a variety of cellular processes causing reduced tumor cell proliferation. Taken together, MYC induces and maintains a tumor cell-specific global 5mC and 5hmC patterns through control of DNMT and TET expression

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