Circadian rhythms: influence on skin cancer and exposure paradigms
Main Article Content
Abstract
Approximately 10% of genes oscillate according to a circadian clock. Even though cells are capable of independent oscillation there is a master controller in the brain, the suprachiasmatic nucleus (SCN), that provides a coordinated response throughout the body, influenced by daily and seasonal patterns of light and heat. These genes have widely varied functions but are significantly influential in DNA damage repair, the cell cycle, cellular proliferation and apoptosis, as well as metabolic function. Normal circadian rhythms are essential for the body’s natural defence against disease and cancer. Deregulation may enhance the capacity for carcinogenesis in the skin and the influence of the circadian clock helps explain two of the anomalies of melanoma exposure patterns: A higher incidence amongst indoor as opposed to outdoor workers and on intermittently as opposed chronically exposed skin.
Article Details
How to Cite
SMITH, David John Mackay.
Circadian rhythms: influence on skin cancer and exposure paradigms.
Medical Research Archives, [S.l.], v. 10, n. 1, jan. 2022.
ISSN 2375-1924.
Available at: <https://esmed.org/MRA/mra/article/view/2672>. Date accessed: 21 nov. 2024.
doi: https://doi.org/10.18103/mra.v10i1.2672.
Section
Review Articles
The Medical Research Archives grants authors the right to publish and reproduce the unrevised contribution in whole or in part at any time and in any form for any scholarly non-commercial purpose with the condition that all publications of the contribution include a full citation to the journal as published by the Medical Research Archives.
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2. Juzeniene, A. & Moan, J. Beneficial effects of UV radiation other than via vitamin D production. 2012. Dermatoendocrinol; 4: 109-117.
3. Hoel, D., Berwick, M., de Gruijl, F., et al. The risks and benefits of sun exposure. 2016. Dermatoendocrinol. 8 e1248325.
4. Van der Rhee, H., DeVries, E., Coelergh, J. Regular sun exposure benefits health. 2016. Med. Hypoth; 97:34-37.
5. Sancar, A., Lindsey-Boltz, L., Gaddameedhi, S., et al. Circadian clock, cancer and chemotherapy. 2015.Biochem; 54: 110-123.
6. Sample, A. & He, Y. Mechanism and prevention of UV-induced melanoma. 2018. Photodermatol/ photoimmunity/photomedicine; 34(1): 13-24.
7. Geyfman, M. et al. Brain and muscle Arnt-like protein-1 (BMAL1) controls circadian cell proliferation and susceptibility to UVB-induced DNA damage in the epidermis. 2012. Proc. Nat. Acad. Sci. USA; 109: 11758-11763.
8. Al-Nuaimi, Y., Hardman, J., Biro, T., et al. A meeting of two chronobiological systems: circadian proteins Period1 and BMAL1 modulate the human hair cycleclock. 2014. J. Invest. Dermatol; 134: 610-619.
9. Takahashi, J. Transcriptional architecture of the mammalian circadian clock. 2017. Nature Reviews, Genetics; 18(3): 164-179.
10. Dibner, C., Schibler, U., Albrecht, U. The mammalian circadian timing system: Organisation and coordination of central and peripheral clocks. 2020. Annu. Rev. Physiol.; 72: 517-549.
11. Sarkar, S.& Gaddameedhi, S. Solar ultraviolet-induced DNA damage response: Melanocytes story in transformation to environmental melanomagenesis. 2020. Environ. Mol. Mutagen; 61: 736-751.
12. Reardon, J. & Sancar, A. Nucleotide excision repair. 2005. Progress in Nucleic acid Res. and Molec. Biol;79: 183-235.
13. Scharer, O. Nucleotide excision repair in eukaryotes. 2013. Cold Springs Harbor Persp. in Biol; 5(10): a012609.
14. Gaddameedhi, S., Selby, C., Kaufmann, W., et al. Control of skin cancer by the circadian rhythm. 2011. PNAS; 108(46): 18790-18795.
15. Sancar, A., Lindsay-Boltz, L., Kang, T., et al. Circadian clock control of the cellular response to DNA damage. 2010. FEBS letters; 584:2618-2625.
16. Sarkar, S., Gaddameedhi, S. UV-B-induced erythema in human skin: the circadian clock is ticking. 2018. J. Invest. Dermatol; 138:248-251.
17. Manzella, N., Bracci, M., Strafella, E., et al. Circadian modulation of 8-oxo guanine DNA damage repair. 2015. Sci. Rep. 5 13752; doi: 10.1038/srep13752.
18. Bradford, P., Goldstein, A., Tamara, D. et al. Cancer and neurological degeneration in Xeroderma Pigmentosum: long term follow-up characterises the role of DNA repair. 2011. J. Med. Genetics; 48(3): 168-176.
19. Imokawa, G. Autocrine and paracrine regulation of melanocytes in human skin and pigmentary disorders. 2004. Pig. Cell Res; 17(2): 9): 6-110.
20. Jarrett, S., Wolf Horrell, E., Christian, P., et al. PKA-mediated phosphorylation of ATR promotes recruitment of XPA to UV-induced DNA damage. 2014. Molec. Cell; 54(6): 999-1011.
21. Kadekaro. A., Leachman, S., Kavanagh, R. et al. Melanocortin 1 receptor genotype: an important determinant of damage response of melanocytes to ultraviolet radiation. 2010. The FASEB J; 24(10): 3850-3860.
22. Smith, D. The melanocortin 1 receptor and its influence on naevi and melanoma in dark-skinned phenotypes. 2018. Aust. J Dermatol. Doi:10.1111/ajd.12982.
23. Schuch, A., Moreno, N., Schuch, N., et al. Sunlight damage to cellular DNA: focus on oxidatively generated lesions. 2013. Free Radical Biol. and Med.; 107:110-124.
24. Masri, S., Cervantes, M., Sassone-Corsi, P. The circadian clock and cell cycle: interconnected biological circuits. 2013. Current Opinion in Cell Biol; 25: 730-734.
25. Bjarnsoon, G., Jordan, R., Wood, P., et al. Circadian expression of clock genes in human oral mucosa and skin: association with specific cell-cycle phases. 2001. Am. J. of Path; 158(5): 1793-1801.
26. Laranjeiro, R., Tamal, K., Peyric, E. et al. Cyclin-dependent kinase inhibitor p20 controls circadian cell-cycle timing. 2013. PNAS; 110(17): 6835-6840.
27. Matsuo, T. et al. Control mechanisms of the circadian clock for timing of cell division in vivo. 2003. Science; 302: 255-259.
28. Geyfman, M. et al. Brain and muscle Arnt-like protein-1 (BMAL1) controls circadian cell proliferation and susceptibility to UVB-induced DNA damage in the epidermis. 2012. Proc. Nat. Acad. Sci. USA; 109: 11758-11763.
29. Grechez-Cassian, A., Rayet, B., Guillaumond, F. et al. The circadian clock component BMAL1 is a critical regulator of p21 WAF1/CIP1 expression and hepatocyte proliferation. 2008. J. Biol. Chem; 283: 4535-4542.
30. Nagoshi, E. et al. Circadian gene expression in individual fibroblasts: cell-autonomous and self-sustained oscillators pass time to daughter cells. 2004. Cell; 119: 693-705.
31. Kowalska, E. NONO couples the circadian clock to the cell cycle. 2012. Proc. Natl. Acad. Sci. USA; 110: 1592-1599.
32. Hyup, J & Sancar, A. Regulation of apoptosis by the circadian clock though NF-𝜅B signalling. 2011. PNAS; 108(29): 12036-12041.
33. Quay, W. Circadian and estrous rhythms in pineal melatonin and 5-hydroxyl indol-3-acetic acid. 1964. Proc. Soc. Exp. Biol. Med; 115:710-713.
34. Fischer, T., Sweatman, I., Semak, R., et al. Constitutive and UV-induced metabolism of melatonin in keratinocytes and cell-free systems. 2006. FASEB. J; 20: 1564-1566.
35. Fischer, T., Zbytek, R., Sayne, E., et al. Melatonin increases survival of HaCaT keratinocytes by suppressing UV-induced apoptosis. 2006. J. Pineal Res: 40: 18-26.
36. Chang, y., Barrett, T., Bishop, D et al. Sun exposure and melanoma risk at different latitudes: a pooled analysis of 5700 cases and 7216 controls. 2009. Int. J. Epidemiol; 38:814-830.
37. Gandini, S., Sera, F., Cattaruzza, M., et al. Meta-analysis of risk factors cutaneous melanoma II sun exposure. 2005. Euro. J. Cancer; 41: 45-60.
38. Reichrath, J., Rech, M., Moeini, M., et al. In vitro comparison to the endocrine system in 1,25(OH)2D3-responsive and -resistant melanoma cells. 2007. Cancer Biol. Ther; 6: 48-55.
39. Newton-Bishop, J., Beswick, S., Randerson-Moor, J., et al. Serum 25 hydroxyvitamin D3 levels are associated with Breslow thickness at presentation and survival from melanoma. 2009. J. Clinic. Oncol; 27: 5439-5444.
40. Nümberg, B., Gröber, S., Gärtner, B., et al. Reduced serum 25OH vitamin D levels in stage IV melanoma patients. 2009. Anticancer Res; 29: 3669-74.
41. Fields, S., Davies, J., Bishop, T., et al. Vitamin D and melanoma. 2013. Dermatol.-Endo; 5(1): 121-129.