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Oncostatic activities of melatonin: Roles in cell cycle, apoptosis, and autophagy.

Abstract
Melatonin, the major secretory product of the pineal gland, not only regulates circadian rhythms, mood, and sleep but also has actions in neoplastic processes which are being intensively investigated. Melatonin is a promising molecule which considered a differentiating agent in some cancer cells at both physiological and pharmacological concentrations. It can also reduce invasive and metastatic status through receptors MT1 and MT2 cytosolic binding sites, including calmodulin and quinone reductase II enzyme, and nuclear receptors related to orphan members of the superfamily RZR/ROR. Melatonin exerts oncostatic functions in numerous human malignancies. An increasing number of studies report that melatonin reduces the invasiveness of several human cancers such as prostate cancer, breast cancer, liver cancer, oral cancer, lung cancer, ovarian cancer, etc. Moreover, melatonin's oncostatic activities are exerted through different biological processes including antiproliferative actions, stimulation of anti-cancer immunity, modulation of the cell cycle, apoptosis, autophagy, the modulation of oncogene expression, and via antiangiogenic effects. This review focuses on the oncostatic activities of melatonin that targeted cell cycle control, with special attention to its modulatory effects on the key regulators of the cell cycle, apoptosis, and telomerase activity.
AuthorsNiloufar Targhazeh, Russel J Reiter, Mahdi Rahimi, Durdi Qujeq, Tooba Yousefi, Mohammad Hassan Shahavi, Seyed Mostafa Mir
JournalBiochimie (Biochimie) Vol. 202 Pg. 34-48 (Nov 2022) ISSN: 1638-6183 [Electronic] France
PMID35752221 (Publication Type: Review, Journal Article)
CopyrightCopyright © 2022 Elsevier B.V. and Société Française de Biochimie et Biologie Moléculaire (SFBBM). All rights reserved.
Chemical References
  • Melatonin
Topics
  • Humans
  • Melatonin (pharmacology, metabolism)
  • Apoptosis
  • Neoplasms (drug therapy, pathology)
  • Autophagy
  • Cell Cycle

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