MYC
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Location (UCSC) | Chr 8: 127.74 – 127.74 Mb | Chr 15: 61.86 – 61.86 Mb | |||||||
PubMed search | [3] | [4] |
View/Edit Human | View/Edit Mouse |
MYC proto-oncogene, bHLH transcription factor is a
Function
This gene is a
As a drug target
Under normal circumstances, c-Myc through its bHLHZip domain heterodimerizes with other transcription factors such as MAD, MAX, and MNT. Myc/Max dimers activate gene transcription, while Mad/Max and Mnt/Max dimers inhibit the activity of Myc.[6] c-MYC is over expressed in the majority of human cancers and in cancers where it is overexpressed, it drives proliferation of cancer cells.[7][8]
A recombinant form of c-Myc called Omomyc in which four residues are mutated has been produced.
The Omomyc displays high affinity for MAX (Myc-associated protein X) and for enhancer box element CACGTG DNA sequences, that result in the uncoupling of cellular proliferation from normal growth factor regulation and contribute to many of the phenotypic hallmarks of cancer.[11] Omomyc also can bind MYC monomers and prevent it entering the nucleus.[12]
The recombinantly produced Omomyc miniprotein has been developed as a drug (OMO-103) and is currently in clinical trials.[13]
References
- ^ a b c GRCh38: Ensembl release 89: ENSG00000136997 – Ensembl, May 2017
- ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000022346 – Ensembl, May 2017
- ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
- ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
- ^ "MYC MYC proto-oncogene, bHLH transcription factor [ Homo sapiens (human) ]". Retrieved 2020-03-02.
- S2CID 4326525.
- PMID 33397405.
- PMID 34508258.
- ^ S2CID 22684888.
- PMID 18716624.
- PMID 32260326.
- PMID 31501275.
- ^ "Results revealed from phase I clinical trial of the first drug to successfully inhibit the MYC gene, which drives many common cancers". European Organisation for. Research and Treatment of Cancer. 25 October 2022 – via EurekAlert!.
Further reading
- Hann SR, King MW, Bentley DL, Anderson CW, Eisenman RN (January 1988). "A non-AUG translational initiation in c-myc exon 1 generates an N-terminally distinct protein whose synthesis is disrupted in Burkitt's lymphomas". Cell. 52 (2): 185–95. S2CID 3012009.
- Hiyama T, Haruma K, Kitadai Y, Ito M, Masuda H, Miyamoto M, Tanaka S, Yoshihara M, Sumii K, Shimamoto F, Chayama K (2001). "c-myc gene mutation in gastric mucosa-associated lymphoid tissue (MALT) lymphoma and diffuse large B-cell lymphoma". Oncol. Rep. 8 (2): 289–92. PMID 11182042.
- Ruf IK, Rhyne PW, Yang H, Borza CM, Hutt-Fletcher LM, Cleveland JL, Sample JT (2001). "EBV Regulates c-MYC, Apoptosis, and Tumorigenicity in Burkitt's Lymphoma". Epstein-Barr Virus and Human Cancer. Current Topics in Microbiology and Immunology. Vol. 258. pp. 153–60. )
- Hu HM, Arcinas M, Boxer LM (March 2002). "A Myc-associated zinc finger protein-related factor binding site is required for the deregulation of c-myc expression by the immunoglobulin heavy chain gene enhancers in Burkitt's lymphoma". J. Biol. Chem. 277 (12): 9819–24. PMID 11777933.
- Hilker M, Tellmann G, Buerke M, Moersig W, Oelert H, Lehr HA, Hake U (2001). "Expression of the proto-oncogene c-myc in human stenotic aortocoronary bypass grafts". Pathol. Res. Pract. 197 (12): 811–6. PMID 11795828.
- Feng XH, Liang YY, Liang M, Zhai W, Lin X (January 2002). "Direct interaction of c-Myc with Smad2 and Smad3 to inhibit TGF-beta-mediated induction of the CDK inhibitor p15(Ink4B)". Mol. Cell. 9 (1): 133–43. PMID 11804592.
- Kuschak TI, Kuschak BC, Taylor CL, Wright JA, Wiener F, Mai S (January 2002). "c-Myc initiates illegitimate replication of the ribonucleotide reductase R2 gene". Oncogene. 21 (6): 909–20. PMID 11840336.
- Chettab K, Zibara K, Belaiba SR, McGregor JL (January 2002). "Acute hyperglycaemia induces changes in the transcription levels of 4 major genes in human endothelial cells: macroarrays-based expression analysis". Thromb. Haemost. 87 (1): 141–8. S2CID 22124540.
This article incorporates text from the United States National Library of Medicine, which is in the public domain.