The c‐myc Promoter: Still MysterY and Challenge
Abstract
The transcription factor c-Myc is a key regulator of cell proliferation, cell growth, differentiation, and apoptosis. Deregulated c-myc expression possesses a high transformation potential and the proto-oncogene c-myc represents a promising target in anticancer therapy. This review on the c-myc promoter describes its organization, the different levels of its normal regulation (including initiation and elongation of transcription, the dual P1/P2 promoters, chromatin structure, c-Myc autosuppression) as well as its deregulation in Burkitt's lymphoma. Furthermore, it summarizes the many different transcription factors, signal transduction pathways, and feedback loops that activate or repress c-myc transcription. Finally, a concept for regulation of the c-myc promoter in different biological settings, for example, immediate-early induction, constant expression throughout the cell cycle in continuously cycling cells, repression during terminal differentiation and deregulation in cancer, is formulated.
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β-catenin has been shown to stimulate c-Myc expression by activating the c-Myc promoter, which comprises multiple T cell factor-4 (TCF-4) binding sites.
“Moreover, β-catenin has been shown to stimulate c-Myc expression by activating the c-Myc promoter, which comprises multiple T cell factor-4 (TCF-4) binding sites.447”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [447]
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Duncan, J. S., Whittle, M. C., Nakamura, K., Abell, A. N., Midland, A. A., Zawistowski, J. S., Johnson, N. L., Granger, D. A., Jordan, N. V., Darr, D. B., et al. (2012) · Cell · doi:10.1016/j.cell.2012.02.053 · Cited by 732 · see citing works
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Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials
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Carabet, L. A., Rennie, P. S., & Cherkasov, A. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms20010120 · Cited by 172 · see citing works
“While being essential for normal Myc regulation in minimizing undesired Myc expression, the integrated biological output from the multiple-input signaling networks poses the risks of driving pathological conditions [33].”
BackgroundInfluentialLiu, O.-G., Xiong, X.-Y., Li, C.-M., Zhou, X.-S., & Li, S.-S. (2018) · Medical Science Monitor · doi:10.12659/msm.905319 · Cited by 4 · see citing works
- Authors
- Wierstra, I., & Alves, J.
- Affiliations
- Medizinische Hochschule Hannover (DE)
- Corresponding author
- Inken Wierstra
- Venue
- Advances in Cancer Research
- Publisher
- Elsevier
- Published
- 2008
- Volume
- 99
- Pages
- 113-333
- ISSN
- 0065-230X (ISSN-L)
- OpenAlex
- W1870041030
- Cited by
- 211
- References
- 1,275
- Citations by year
- 2025: 6 · 2024: 5 · 2023: 9 · 2022: 8 · 2021: 9 · 2020: 18 · 2019: 12 · 2018: 11 · 2017: 16 · 2016: 11 · 2015: 9 · 2014: 12 · 2013: 17 · 2012: 13
- FWCI
- 15.49
- Type
- book chapter
- Language
- en
- Open access
- closed
- Locations
- Advances in cancer research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Health Sciences › Medicine › Pathology and Forensic Medicine › Lymphoma Diagnosis and Treatment
- Keywords
- c-Myc, c-myc promoter, transcriptional regulation, chromatin structure, Burkitt lymphoma, proto-oncogenes, signaling pathways, transcription factors, cell cycle, terminal differentiation
- MeSH terms
- Proto-Oncogene Mas, Animals, Burkitt Lymphoma, Chromatin, Gene Expression Regulation, Humans, Neoplasms, Promoter Regions, Genetic, Proto-Oncogenes, Repressor Proteins, Transcription Factors, Signal Transduction, Genes, myc
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