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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]