Molecular and epigenetic effects of Melatonin in Breast Cancer

Numerous studies have demonstrated the oncostatic properties of melatonin both in vivo using models of chemically induced rat mammary tumors as well as in vitro using MCF-7 human breast cancer cells. Melatonin exerts both inhibitory as well proapoptotic effects by interacting with several molecular pathways. Generally, melatonin’s cytostatic effects are mediated by interactions of the indoleamine with both ERs and melatonin receptors. However, recently some receptor- and estrogen-independent signaling pathways activated by melatonin have been discovered. In particular, increasing attention should be directed to melatonin’s effects on the cytoskeleton and cell shape, as well as understanding how melatonin could inhibit both Akt activation and MAPK-related pathways. In lights of its low toxicity melatonin, either alone or in combination with chemoradiotherapy, should be considered as a potentially new anticancer treatment. There may be some difficulties in bringing a circadian rhythm-based melatonin chronotherapy to cancer clinics, but it is a challenge to use this indoleamine to derive its benefit in the practice of oncology.