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. Author manuscript; available in PMC: 2020 Mar 1.
Published in final edited form as: Biochim Biophys Acta Gene Regul Mech. 2018 Oct 5;1862(3):382–393. doi: 10.1016/j.bbagrm.2018.09.010

Figure 4: m6A-dependent pathways regulate control of cellular transcription factors.

Figure 4:

(A) Mutations in IDH lead to the production of the onco-metabolite 2-hydroxyglutarate (2HG). Accumulation of 2HG inhibits the activity of the m6A demethylase FTO, leading to downregulation of MYC and suppressed MYC signaling. (B) Upregulation of METTL14 in individuals with acute myeloid leukemia (AML) leads to increased deposition of m6A. Stabilization of MYC mRNA, through interaction with an unknown reader protein, drives a self-renewal phenotype in the cancer cells; (C) In cervical cancer and hepatocellular carcinoma (HCC) cells, the m6A reader IGFB2BP stabilizes MYC mRNA, leading to increased cellular proliferation; (D) In glioblastoma cells, the lncRNA FOXM1-AS mediates the interaction between HuR and the demethylase ALKBH5, increasing expression of the transcription factor FOXM1 and driving a self-renewal phenotype. (E) Translation of the transcription factor HIF-1α is promoted by the m6A reader YTHDC2. HIF activates the transcription of genes that play a role in angiogenesis and adaptive response.