Table 5.
Partial regulators or inhibitors of m6A modifications may provide the potential therapeutic strategies in cancer treatment
| 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 BC |
Prevent or override tyrosine kinase inhibitor resistance Decrease tumor growth |
[149] [94] |
| 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] |
GBM glioblastoma; AML acute myeloid leukemia; BC breast cancer; CRC colorectal cancer