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Table 1 Typical examples of drug re-positioning targeting Myc in tumor cells

From: Emerging roles of Myc in stem cell biology and novel tumor therapies

Name of the agent Conventional applications Mechanisms of action References
Valproic acid (a short-chain fatty acid HDAC inhibitor) Migraine attacks, depression and epilepsy such as tonic-clonic seizures To upregulate CDKN1A/B (p21, p27) and downregulate c-Myc, thereby inducing autophagic cell death in cutaneous T cell lymphoma and Burkitt lymphoma [75, 76]
Retinoic acid (an analogue of vitamin A) Acne vulgaris, psoriasis, and AML M3 (acute promylocytic leukemia; APL) To downregulate N-Myc in cooperation with interferon-γ (IFN-γ), thereby inducing differentiation in neuroblastoma [85, 232, 233]
Bortezomib (proteasome inhibitor) Multiple myeloma To up-regulate the proapoptotic protein NOXA in malignant melanoma and Burkitt lymphoma directly dependent on c-MYC [234, 235]
Sulfasalazine (cystine/glutamate antiporter inhibitor) Ulcerative colitis and rheumatoid arthritis To disrupt the circadian rhythm of transferrin receptor 1 gene expression regulated by c-Myc and to decrease glutathione synthesis by the inhibition of cystine uptake via system Xc(-) [117, 130, 236]