Abstract
Breast cancer is the most common type of cancer. In the developmental stages of breast cancer, estrogens are strongly involved. As estrogen synthesis is regulated by the enzyme aromatase, targeting the activity of this enzyme represents a therapeutic option. The pineal hormone melatonin may exert a suppressive role on aromatase activity, leading to reduced estrogen biosynthesis. A melatonin-mediated decrease in the expression of aromatase promoters and associated genes would provide suitable evidence of this molecule’s efficacy as an aromatase inhibitor. Furthermore, melatonin intensifies radiation-induced anti-aromatase effects and counteracts the unwanted disadvantages of chemotherapeutic agents. In this manner, this review summarizes the inhibitory role of melatonin in aromatase action, suggesting its role as a possible oncostatic molecule in breast cancer.
Highlights
Excessive expression of aromatase resulting from aromatase promoter I.7 in vascular endothelial tissue adjacent to cancerous breast tissue causes the development of breast tumors via the following two mechanisms: (1) Peripheral estrogen levels may be increased by excessive aromatase activity, leading to direct tumoral growth
The MT1 melatonin receptor is reportedly expressed in the estrogen receptor-positive human breast cancer cell line MCF7, which is sensitive to melatonin-mediated antiproliferation and anti-aromatase effects [26,75]
The suppression of estrogen synthesis is fundamental for breast cancer therapy, due to the strong link between estrogen and breast cancer progression
Summary
Since the enzyme aromatase is in charge of estrogen biosynthesis, estrogen-associated genes are known to be downregulated when this enzyme is inhibited [3] Inhibitors of this enzyme have been considered to be effective targeted therapies for breast cancer. Melatonin is able to protect normal cells from the cytotoxicity accompanied by ionizing radiation (IR) This non-targeted effect following IR is alleviated via melatonin-mediated regulation of prostaglandins, Toll-like receptors (TLRs), and transcription factors [24]. Multiple researchers have found receptor-targeted cancer therapies to be effective, and their transaction with melatonin would be beneficial [29,30] In this respect, this review aimed to summarize recent findings related to the melatonin-induced inhibition of aromatase and the resultant growth suppression of hormone-dependent breast tumors
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