The Redox Role of G6PD in Cell Growth, Cell Death, and Cancer

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Abstract

The generation of reducing equivalent NADPH via glucose-6-phosphate dehydrogenase (G6PD) is critical for the maintenance of redox homeostasis and reductive biosynthesis in cells. NADPH also plays key roles in cellular processes mediated by redox signaling. Insufficient G6PD activity predisposes cells to growth retardation and demise. Severely lacking G6PD impairs embryonic development and delays organismal growth. Altered G6PD activity is associated with pathophysiology, such as autophagy, insulin resistance, infection, inflammation, as well as diabetes and hypertension. Aberrant activation of G6PD leads to enhanced cell proliferation and adaptation in many types of cancers. The present review aims to update the existing knowledge concerning G6PD and emphasizes how G6PD modulates redox signaling and affects cell survival and demise, particularly in diseases such as cancer. Exploiting G6PD as a potential drug target against cancer is also discussed.

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G Kroemer, L Galluzzi, P Vandenabeele … (2009)

Different types of cell death are often defined by morphological criteria, without a clear reference to precise biochemical mechanisms. The Nomenclature Committee on Cell Death (NCCD) proposes unified criteria for the definition of cell death and of its different morphologies, while formulating several caveats against the misuse of words and concepts that slow down progress in the area of cell death research. Authors, reviewers and editors of scientific periodicals are invited to abandon expressions like 'percentage apoptosis' and to replace them with more accurate descriptions of the biochemical and cellular parameters that are actually measured. Moreover, at the present stage, it should be accepted that caspase-independent mechanisms can cooperate with (or substitute for) caspases in the execution of lethal signaling pathways and that 'autophagic cell death' is a type of cell death occurring together with (but not necessarily by) autophagic vacuolization. This study details the 2009 recommendations of the NCCD on the use of cell death-related terminology including 'entosis', 'mitotic catastrophe', 'necrosis', 'necroptosis' and 'pyroptosis'.

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A. G. Bodnar, M. Ouellette, M Frolkis … (1998)

Normal human cells undergo a finite number of cell divisions and ultimately enter a nondividing state called replicative senescence. It has been proposed that telomere shortening is the molecular clock that triggers senescence. To test this hypothesis, two telomerase-negative normal human cell types, retinal pigment epithelial cells and foreskin fibroblasts, were transfected with vectors encoding the human telomerase catalytic subunit. In contrast to telomerase-negative control clones, which exhibited telomere shortening and senescence, telomerase-expressing clones had elongated telomeres, divided vigorously, and showed reduced straining for beta-galactosidase, a biomarker for senescence. Notably, the telomerase-expressing clones have a normal karyotype and have already exceeded their normal life-span by at least 20 doublings, thus establishing a causal relationship between telomere shortening and in vitro cellular senescence. The ability to maintain normal human cells in a phenotypically youthful state could have important applications in research and medicine.

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H2S as a physiologic vasorelaxant: hypertension in mice with deletion of cystathionine gamma-lyase.

Guangdong Yang, Lingyun Wu, Bo Jiang … (2008)

Studies of nitric oxide over the past two decades have highlighted the fundamental importance of gaseous signaling molecules in biology and medicine. The physiological role of other gases such as carbon monoxide and hydrogen sulfide (H2S) is now receiving increasing attention. Here we show that H2S is physiologically generated by cystathionine gamma-lyase (CSE) and that genetic deletion of this enzyme in mice markedly reduces H2S levels in the serum, heart, aorta, and other tissues. Mutant mice lacking CSE display pronounced hypertension and diminished endothelium-dependent vasorelaxation. CSE is physiologically activated by calcium-calmodulin, which is a mechanism for H2S formation in response to vascular activation. These findings provide direct evidence that H2S is a physiologic vasodilator and regulator of blood pressure.

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Journal ID (nlm-ta): Cells

Journal ID (iso-abbrev): Cells

Journal ID (publisher-id): cells

Title: Cells

Publisher: MDPI

ISSN (Electronic): 2073-4409

Publication date (Electronic): 08 September 2019

Publication date Collection: September 2019

Volume: 8

Issue: 9

Electronic Location Identifier: 1055

Affiliations

[1 ]Department of Medical Laboratory Science and Biotechnology, Yuanpei University of Medical Technology, Hsinchu 30041, Taiwan

[2 ]Research Center for Chinese Herbal Medicine, College of Human Ecology, Chang Gung University of Science and Technology, Taoyuan 33043, Taiwan; yhwu03@ 123456mail.cgust.edu.tw

[3 ]Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taoyuan 33043, Taiwan; d56610@ 123456yahoo.com.tw

[4 ]Department of Medical Biotechnology and Laboratory Sciences, College of Medicine, Chang Gung University, Taoyuan 33043, Taiwan; liuhy@ 123456mail.cgu.edu.tw

[5 ]Research Center for Food and Cosmetic Safety, College of Human Ecology, Chang Gung University of Science and Technology, Taoyuan 33043, Taiwan; htl@ 123456mail.cgu.edu.tw

[6 ]Graduate Institute of Natural Products, College of Medicine, Chang Gung University, Taoyuan 33043, Taiwan

[7 ]Chinese Herbal Medicine Research Team, Healthy Aging Research Center, Chang Gung University, Taoyuan 33043, Taiwan

[8 ]Department of Anaesthesiology, Chang Gung Memorial Hospital, Taoyuan 33043, Taiwan

[9 ]Department of Chemical Engineering, Ming Chi University of Technology, New Taipei City 24301, Taiwan

[10 ]Research Center for Chinese Herbal Medicine, Graduate Institute of Health Industry Technology, College of Human Ecology, Chang Gung University of Science and Technology, Taoyuan 33043, Taiwan

[11 ]School of Medicine, New York University, New York, NY 10016, USA; stern@ 123456nyulangone.org

[12 ]Department of Pediatric Hematology/Oncology, Linkou Chang Gung Memorial Hospital, Taoyuan 33043, Taiwan

[13 ]Healthy Aging Research Center, Chang Gung University, Taoyuan 33043, Taiwan

Author notes

[* ]Correspondence: hcyang@ 123456mail.ypu.edu.tw (H.-C.Y.); dtychiu@ 123456mail.cgu.edu.tw (D.T.-Y.C.); Tel.: +886-3-6108175 (H.-C.Y.); +886-3-2118800 (ext. 5097) (D.T.-Y.C.); Fax: +886-3-6102327 (H.-C.Y.); +886-3-2118540 (D.T.-Y.C.)

[†]

These authors contributed equally to this work.

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Tsong-Long Hwang https://orcid.org/0000-0002-5780-3977

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Publisher ID: cells-08-01055

DOI: 10.3390/cells8091055

PMC ID: 6770671

PubMed ID: 31500396

SO-VID: 156af8fd-8c35-47a9-94a0-1d2f36bf094c

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Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

The Redox Role of G6PD in Cell Growth, Cell Death, and Cancer

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Gamma Delta T cells

Most cited references 201

Classification of cell death: recommendations of the Nomenclature Committee on Cell Death 2009.

Extension of life-span by introduction of telomerase into normal human cells.

H2S as a physiologic vasorelaxant: hypertension in mice with deletion of cystathionine gamma-lyase.

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