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Therapeutic potential of melatonin in colorectal cancer: Focus on lipid metabolism and gut microbiota
Open accessAbstract
Colorectal cancer (CRC) is one of the most common gastrointestinal malignancies. The occurrence and development of CRC are complicated processes. Obesity and dysbacteriosis have been increasingly regarded as the main risk factors for CRC. Understanding the etiology of CRC from multiple perspectives is conducive to screening for some potential drugs or new treatment strategies to limit the serious side effects of conventional treatment and prolong the survival of CRC patients. Melatonin, a natural indoleamine, is mainly produced by the pineal gland, but it is also abundant in other tissues, including the gastrointestinal tract, retina, testes, lymphocytes, and Harder's glands. Melatonin could participate in lipid metabolism by regulating adipogenesis and lipolysis. Additionally, many studies have focused on the potential beneficial effects of melatonin in CRC, such as promotion of apoptosis; inhibition of cell proliferation, migration, and invasion; antioxidant activity; and immune regulation. Meaningfully, gut microbiota is the main determinant of all aspects of health and disease (including obesity and tumorigenesis). The gut microbiota is of great significance for understanding the relationship between obesity and increased risk of CRC. Although the current understanding of how the melatonin-mediated gut microbiota coordinates a variety of physiological and pathological activities is fairly comprehensive, there are still many unknown topics to be explored in the face of a complex nutritional status and a changeable microbiota. This review summarizes the potential links among melatonin, lipid metabolism, gut microbiota, and CRC to promote the development of melatonin as a preventive and therapeutic agent for CRC.
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“Numerous metabolic pathways in adipose tissue, like the induction and discouragement of adipokines, are controlled by circadian rhythm that is partly regulated by melatonin, which may act on WAT through MT1 and MT2 or using the sympathetic nervous system. 3,11,12”
From Melatonin supplementation improves glycemic hemostasis, lipid profile, and adipokine concentrations of obese women: A double-blind randomized clinical trial (2024) · cites this paper as [12]
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Metadata
- Authors
- Pan, S., Guo, Y., Hong, F., Xu, P., & Zhai, Y.
- Affiliations
- Beijing Normal University (CN)
- University of Pittsburgh (US)
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
- Publisher
- Elsevier BV
- Published
- 2022-01
- Volume
- 1868
- Issue
- 1
- Pages
- 166281
- ISSN
- 0925-4439 (ISSN-L)
- OpenAlex
- W3204951023
- Cited by
- 37
- References
- 241
- Citations by year
- 2026: 6 · 2025: 7 · 2024: 9 · 2023: 7 · 2022: 6
- FWCI
- 0.73
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 365 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (31571164, 82070901)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Physiology (medical) › Dietary Effects on Health
- Keywords
- melatonin, colorectal cancer, lipid metabolism, gut microbiota, obesity, dysbiosis, adipogenesis, lipolysis, apoptosis, cell proliferation, antioxidant activity, immune regulation, cancer prevention, cancer therapy
- MeSH terms
- Gastrointestinal Microbiome, Cell Movement, Humans, Melatonin, Neoplasm Invasiveness, Colorectal Neoplasms, Apoptosis, Cell Proliferation, Lipid Metabolism, Carcinogenesis
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