Cell cycle involvement in cancer therapy; WEE1 kinase, a potential target as therapeutic strategy.

Autor:	Vakili-Samiani S; Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran; Medical Education Research Center, Health Management and Safety Promotion Research Institute, Tabriz University of Medical Sciences, Tabriz, Iran; Hematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Educational Development Center, Department of Medical Education, Tabriz University of Medical Sciences, Tabriz, Iran; Educational Development Organization, Department of Medical Education, Tabriz University of Medical Sciences, Tabriz, Iran. Electronic address: Vakilis@tbzmed.ac.ir., Khanghah OJ; Department of Biochemistry and Clinical Laboratories, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran., Gholipour E; Hematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran., Najafi F; Educational Development Center, Department of Medical Education, Tabriz University of Medical Sciences, Tabriz, Iran., Zeinalzadeh E; Hematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran., Samadi P; Educational Development Center, Department of Medical Education, Tabriz University of Medical Sciences, Tabriz, Iran; Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran., Sarvarian P; Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran., Pourvahdani S; Hematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran., Kelaye SK; Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran., Hamblin MR; Laser Research Centre, Faculty of Health Science, University of Johannesburg, Doornfontein, Johannesburg 2028 South Africa; Radiation Biology Research Center, Iran University of Medical Sciences, Tehran, Iran., Feizi AAH; Hematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. Electronic address: pourfeizi@yahoo.com.
Jazyk:	angličtina
Zdroj:	Mutation research [Mutat Res] 2022 Jan-Jun; Vol. 824, pp. 111776. Date of Electronic Publication: 2022 Feb 19.
DOI:	10.1016/j.mrfmmm.2022.111776
Abstrakt:	Mitosis is the process of cell division and is regulated by checkpoints in the cell cycle. G1-S, S, and G2-M are the three main checkpoints that prevent initiation of the next phase of the cell cycle phase until previous phase has completed. DNA damage leads to activation of the G2-M checkpoint, which can trigger a downstream DNA damage response (DDR) pathway to induce cell cycle arrest while the damage is repaired. If the DNA damage cannot be repaired, the replication stress response (RSR) pathway finally leads to cell death by apoptosis, in this case called mitotic catastrophe. Many cancer treatments (chemotherapy and radiotherapy) cause DNA damages based on SSBs (single strand breaks) or DSBs (double strand breaks), which cause cell death through mitotic catastrophe. However, damaged cells can activate WEE1 kinase (as a part of the DDR and RSR pathways), which prevents apoptosis and cell death by inducing cell cycle arrest at G2 phase. Therefore, inhibition of WEE1 kinase could sensitize cancer cells to chemotherapeutic drugs. This review focuses on the role of WEE1 kinase (as a biological macromolecule which has a molecular mass of 96 kDa) in the cell cycle, and its interactions with other regulatory pathways. In addition, we discuss the potential of WEE1 inhibition as a new therapeutic approach in the treatment of various cancers, such as melanoma, breast cancer, pancreatic cancer, cervical cancer, etc. (Copyright © 2022 Elsevier B.V. All rights reserved.)
Databáze:	MEDLINE
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