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Table 5 Partial regulators or inhibitors of m6A modifications may provide the potential therapeutic strategies in cancer treatment

From: Mechanism of RNA modification N6-methyladenosine in human cancer

Drug Role Target Selective Biological function Cancer Effect/ Mechanism on cancer Refs
MA /MA2 Inhibitor FTO Yes Stabilize FTO binding for the m6A-containing nucleic acid GBM Inhibit GSC growth and self-renewal [49]
FB23/FB23–2 Inhibitor FTO Yes Directly bind to FTO and inhibit m6A demethylase activity AML Suppress proliferation and promote the differentiation/apoptosis [148]
Rhein Inhibitor FTO No Binding FTO catalytic domain against ssRNA substrate AML
Prevent or override tyrosine kinase inhibitor resistance
Decrease tumor growth
R-2HG Inhibitor FTO No Suppress FTO activity and elevate m6A RNA modification AML Inhibit proliferation/survival of FTO-high cancer cells [45]
MO-I-500 Inhibitor FTO Yes Purify FTO demethylase catalyzing demethylation BC Inhibit survival of BC cells via decreasing FTO and IRX3 proteins [150]
SPI1 Regulator METTL14 No Negatively regulate METTL14 expression AML Inhibit differentiation via targeting MYB and MYC [42]
CA4 Regulator WTAP No Interact with WTAP and induce WTAP protein degradation CRC Inhibits CRC development through WTAP–WT1–TBL1 axis [73]
  1. GBM glioblastoma; AML acute myeloid leukemia; BC breast cancer; CRC colorectal cancer