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

Anti-cancer Apoptosis Autophagy Cell cycle Melatonin

Journal

Biochimie
ISSN: 1638-6183
Titre abrégé: Biochimie
Pays: France
ID NLM: 1264604

Informations de publication

Date de publication:
23 May 2022
Historique:
received: 14 02 2022
revised: 14 05 2022
accepted: 17 05 2022
pubmed: 27 5 2022
medline: 27 5 2022
entrez: 26 5 2022
Statut: aheadofprint

Résumé

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.

Identifiants

pubmed: 35618158
pii: S0300-9084(22)00129-8
doi: 10.1016/j.biochi.2022.05.008
pii:
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

44-59

Informations de copyright

Copyright © 2022. Published by Elsevier B.V.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare no conflicts of interest.

Auteurs

Niloufar Targhazeh (N)

Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.

Russel J Reiter (RJ)

Department of Cell Systems and Anatomy, University of Texas Health Science Center, San Antonio, TX, USA.

Mahdi Rahimi (M)

Lodz University of Technology, Institute of Polymer and Dye Technology, Stefanowskiego 16, 90-537, Lodz, Poland; International Center for Research on Innovative Biobased Materials (ICRI-BioM)-International Research Agenda, Lodz University of Technology, Lodz, Poland.

Durdi Qujeq (D)

Cellular and Molecular Biology Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran; Department of Clinical Biochemistry, Faculty of Medicine, Babol University of Medical Sciences, Babol, Iran.

Tooba Yousefi (T)

Department of Clinical Biochemistry, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Iran.

Mohammad Hassan Shahavi (MH)

Department of Nanotechnology, Faculty of Engineering Modern Technologies, Amol University of Special Modern Technologies, Amol, Iran.

Seyed Mostafa Mir (SM)

Metabolic Disorders Research Center, Golestan University of Medical Sciences, Gorgan, Iran; Department of Clinical Biochemistry, Faculty of Medicine, Golestan University of Medical Sciences, Babol, Iran. Electronic address: mostafamir1987@gmail.com.

Classifications MeSH