How does Melatonin help to fight cancer?
Studies on the effect of Melatonin on tumor growth and angiogenesis in xenograft model of Breast Cancer revealed that Melatonin reduces tumor growth and cell proliferation and inhibits angiogenesis by decreasing the expression of Vascular Endothelial Growth Factor (VEGF) receptor 2 and increasing the influence of insulin growth factor 1 and epidermal growth factor. Studies also show that the Melatonin hormone participates in the activation of lymphocytes and monocytes/macrophages, preventing tumor development, and fighting against potential carcinogens.
Melatonin is a naturally produced hormone. By controlling circadian rhythms of sleep and wakefulness, Melatonin inhibits the growth of cancer cells, including Breast Cancer and melanoma, when directly applied to the cells. However, under various researches, It is observed that Melatonin is not the hormone to treat cancer in humans; it only improves sleep quality. However, it can also be used to treat specific Chemotherapy repercussions and reduce the side effects of cancer treatments.
Some research also shows that Melatonin’s effects on breast cancer, out of all the other types of cancer, is the most significant because the administration of the hormone in preliminary stages of Breast Cancer has shown a significant antiproliferative effect in Breast Cancer cells in vitro and inhibited the growth of breast tumors in mice.
In conclusion, Melatonin has multiple effects and plays an important role in adhesion, migration, invasion, and apoptosis of cells.
The biomodification of cancer Chemotherapy and Radiotherapy by the administration of Melatonin confirms decreased toxicity and increased efficacy of Cancer Treatment on patients with poor clinical status and solid metastatic tumors.
Controlled trials that examined the relationship between Melatonin levels and neoplastic activity concluded that Melatonin, through its antiproliferative, antioxidative, and immunostimulatory actions, should be considered a naturally oncostatic agent.