The protein encoded by this gene is a multifunctional phosphoprotein that plays a role in cell cycle progression, apoptosis and cellular transformation. It functions as a transcription factor that regulates transcription of specific target genes. Binding of Myc requires dimerization to another protein, namely Max. Myc/Max complexes activate transcription and promote cell proliferation and transformation. Expression of Myc is required for proliferation.
Genetic alteration of MYC is implicated in the etiology of a variety of tumors, including breast, cervical and colon cancers, as well as in squamous cell carcinomas of the head and neck, myeloma, non-Hodgkin's lymphoma, gastric adenocarcinomas and ovarian cancer. MYC gene activation (enhanced expression and/or amplification) may result from chromosomal duplication as well as translocation, and from retroviral as well as point mutation.
Genetic alterations involving MYC are a cause of Burkitt lymphoma (BL), a form of undifferentiated malignant lymphoma commonly manifested as a large osteolytic lesion in the jaw or as an abdominal mass. Translocations t(2;8)(p11;q24), t(8;14)(q24;q32) or t(8;22)(q24;q11) juxtaposing MYC to immunoglobin chains IGK@, IGH@ or IGL@ are usually found in Burkitt lymphoma.
Translocations may also lead to BCL6-MYC (t(3;8)(q27;q24.1)), MYC-ZBTB5 (t(8;9)(q24;p13)), MYC-ZCCHC7 (t(8;9)(q24;p13)), BTG1-MYC (t(8;12)(q21;q22)), TRA@-MYC (t(8;14)(q24;q11)), MYC-BCL3 (t(8;19)(q24;q13.1)) in non-Hodgkin's lymphoma (NHL), chronic lymphocytic leukemia (CLL), B-acute lymphoblastic leukemia (B-ALL) and acute myeloid leukemia (AML).
Despite its pervasive role in human cancer, Myc met with considerable skepticism as a therapeutic target since its requirement for proliferation and maintenance of adult stem cell compartments raised concern about the toxicity of Myc inhibition for healthy tissues. One of the most recent inhibitor is Omomyc, a Myc-interfering molecule. Omomyc action is different from the one that can be obtained by gene knockout or RNA interference, approaches designed to block all functions of a gene product. This molecule – instead – appears to cause an edge-specific perturbation that destroys some protein interactions of the Myc node and keeps others intact, with the result of reshaping the Myc transcriptome (Savino M. et al. 2011)
References (open access):
The action mechanism of the myc inhibitor termed omomyc may give clues on how to target myc for cancer therapy. Savino M, Annibali D, Carucci N, Favuzzi E, Cole MD, Evan GI, Soucek L, Nasi S. PLoS One. 2011;6(7):e22284.
c-Myc induction of programmed cell death may contribute to carcinogenesis: a perspective inspired by several concepts of chemical carcinogenesis. Wang C, Tai Y, Lisanti MP, Liao DJ. Cancer Biol Ther. 2011 Apr 1;11(7):615-26.