Oncomedicine 2018; 3:37-47. doi:10.7150/oncm.25566
The Role of Melatonin in Cancer Development
1. Departments of Biology and Advanced Placement Biology, White Station High School, Memphis, Tennessee 38117. USA.
2. Departments of Biology and Advanced Placement Biology, White Station High School, Memphis, Tennessee 38117. USA.
3. Department of Pathology and Laboratory Medicine, University of Tennessee Health Science Center, Memphis, TN 38163. USA.
Melatonin is a hormone that is secreted by the pineal gland in the brain. Its secretion during periods of darkness represents a 24-hour rhythm controlled by the circadian clock and is pivotal in the regulation of sleep and wake cycles. Although circadian rhythms are endogenous processes, they can be affected by environmental factors such as light and temperature. In addition to its role in circadian rhythms, melatonin has also been observed to function in the immune system, female menstrual cycles, seasonal behavior, tumor inhibition, and anti-aging processes.  Melatonin production increases during the night and decreases in the daytime with exposure to light. Low levels of normal melatonin have been linked to neoplasia, such as the growth of rat hepatomas and human breast cancer xenografts, circadian phase shifts, sleep disturbances, and immunosuppression. [3,4] Furthermore, sleep disturbance, not factoring in melatonin production, can lead to immune suppression and a shift to the predominance in cancer-stimulatory cytokines.  To combat cancer, studies have shown that melatonin significantly suppresses cell proliferation and induces apoptosis.  There have been no direct links determined between abnormal melatonin production observed in sleep disturbances and cancer, so this review will focus on the experimental evidence depicting the role of melatonin in the prevention of cancer development.
Keywords: Melatonin, cancer development
Liu S, Madu CO, Lu Y. The Role of Melatonin in Cancer Development. Oncomedicine 2018; 3:37-47. doi:10.7150/oncm.25566. Available from http://www.oncm.org/v03p0037.htm