Glyoxalase 1 as a Therapeutic Target in Cancer and Cancer Stem Cells.


Journal

Molecules and cells
ISSN: 0219-1032
Titre abrégé: Mol Cells
Pays: Korea (South)
ID NLM: 9610936

Informations de publication

Date de publication:
31 Dec 2022
Historique:
received: 05 07 2022
revised: 29 07 2022
accepted: 01 08 2022
pubmed: 30 9 2022
medline: 29 12 2022
entrez: 29 9 2022
Statut: ppublish

Résumé

Methylglyoxal (MG) is a dicarbonyl compound formed in cells mainly by the spontaneous degradation of the triose phosphate intermediates of glycolysis. MG is a powerful precursor of advanced glycation end products, which lead to strong dicarbonyl and oxidative stress. Although divergent functions of MG have been observed depending on its concentration, MG is considered to be a potential anti-tumor factor due to its cytotoxic effects within the oncologic domain. MG detoxification is carried out by the glyoxalase system. Glyoxalase 1 (Glo1), the ubiquitous glutathione-dependent enzyme responsible for MG degradation, is considered to be a tumor promoting factor due to it catalyzing the removal of cytotoxic MG. Indeed, various cancer types exhibit increased expression and activity of Glo1 that closely correlate with tumor cell growth and metastasis. Furthermore, mounting evidence suggests that Glo1 contributes to cancer stem cell survival. In this review, we discuss the role of Glo1 in the malignant progression of cancer and its possible use as a promising therapeutic target for tumor therapy. We also summarize therapeutic outcomes of Glo1 inhibitors as prospective treatments for the prevention of cancer.

Identifiants

pubmed: 36172978
pii: molcells.2022.0109
doi: 10.14348/molcells.2022.0109
pmc: PMC9794553
doi:

Substances chimiques

Antineoplastic Agents 0
Lactoylglutathione Lyase EC 4.4.1.5

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

869-876

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Auteurs

Ji-Young Kim (JY)

Department of Internal Medicine, School of Medicine, Kangwon National University, Chuncheon 24341, Korea.
These authors contributed equally to this work.

Ji-Hye Jung (JH)

Department of Internal Medicine, School of Medicine, Kangwon National University, Chuncheon 24341, Korea.
These authors contributed equally to this work.

Seung-Joon Lee (SJ)

Department of Internal Medicine, School of Medicine, Kangwon National University, Chuncheon 24341, Korea.

Seon-Sook Han (SS)

Department of Internal Medicine, School of Medicine, Kangwon National University, Chuncheon 24341, Korea.

Seok-Ho Hong (SH)

Department of Internal Medicine, School of Medicine, Kangwon National University, Chuncheon 24341, Korea.
Institute of Medical Science, School of Medicine, Kangwon National University, Chuncheon 24341, Korea.
KW-Bio Co., Ltd., Wonju 26487, Korea.

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