Features of Melatonin Receptor Expression in Endometrial Precancerous and Neoplastic Processes

Melatonin is a multifunctional neuroendocrine hormone produced primarily by the pineal gland and widely recognized for its role in the regulation of circadian rhythms. In addition to its chronobiological function, melatonin exerts a variety of biological effects, including antioxidant activity, immune modulation, regulation of cell proliferation, and induction of apoptosis. These properties have attracted increasing attention in oncology research, particularly in hormone-dependent malignancies. Endometrial carcinoma is one of the most common gynecological cancers worldwide and often develops through a multistep process involving endometrial hyperplasia and progressive molecular changes in endometrial tissue. The pathogenesis of endometrial tumors is strongly influenced by hormonal regulation, particularly through estrogen and progesterone signaling pathways. However, emerging evidence suggests that additional hormonal regulators, including melatonin, may contribute to the complex mechanisms of endometrial carcinogenesis.

Melatonin exerts most of its biological effects through specific membrane receptors, mainly MT1 and MT2, which are expressed in many tissues, including the female reproductive tract. However, the expression patterns and biological significance of melatonin receptors in precancerous and malignant endometrial lesions are still poorly understood. Understanding these relationships may provide important insights into the molecular mechanisms of progression from endometrial hyperplasia to carcinoma. Furthermore, assessment of melatonin receptor expression at different stages of endometrial pathology may help identify novel biomarkers with diagnostic or prognostic value.

A review of the existing literature highlights the potential importance of melatonin receptor signaling in the development and progression of endometrial tumors.