Overexpression of Glucose-6-Phosphate-Dehydrogenase in Rat Hepatic Preneoplasia and Neoplasia

Stumpf, H; Bannasch, Peter

doi:10.3892/ijo.5.6.1255

Cited by 10 publications

(9 citation statements)

References 35 publications

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“…In rat experimental models consisting of normal and regenerating livers and cell lines, G6PD activity was found to be highly increased in the Novikoff hepatoma (68) and in eight rapidly growing hepatomas, but not in the one displaying a slow growth rate (69). An increase in G6PD-positivity in preneoplastic hepatic lesions and HCC, associated with a high labeling index, has been also reported in different studies using a rat protocol of hepatocarcinogenesis induced by N -nitrosomorpholine (70–72). Later on, Frederiks et al showed that diethylnitrosamine (DENA)-induced rat preneoplastic lesions were characterized by a 25-fold increase of G6PD activity when compared with the surrounding tissue (73, 74).…”

Section: G6pd and Hccmentioning

confidence: 55%

Emerging Role of the Pentose Phosphate Pathway in Hepatocellular Carcinoma

2017

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In recent years, there has been a revival of interest in metabolic changes of cancer cells as it has been noticed that malignant transformation and metabolic reprogramming are closely intertwined. The pentose phosphate pathway (PPP) is one of the fundamental components of cellular metabolism crucial for cancer cells. This review will discuss recent findings regarding the involvement of PPP enzymes in several types of cancer, with a focus on hepatocellular carcinoma (HCC). We will pay considerable attention to the involvement of glucose-6-phosphate dehydrogenase, the rate-limiting enzyme of the PPP. Subsequently, we discuss the inhibition of the PPP as a potential therapeutic strategy against cancer, in particular, HCC.

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Section: G6pd and Hccmentioning

confidence: 55%

Emerging Role of the Pentose Phosphate Pathway in Hepatocellular Carcinoma

2017

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“…In addition, G6PDH is a regulatory enzyme in NADPH-dependent xenobiotic biotransformation and defenses against oxidative damage and is very sensitive to inactivation by chronic exposure to pollutants in highly contaminated marine habitats. Moreover, focal alterations in its activity provide a sensitive histochemical parameter to detect early stages of xenobiotic-induced hepatocellular carcinogenesis in humans and rodents before morphological changes appear (Stumpf and Bannasch, 1994). Therefore, G6PDH is not only a relevant experimental marker for carcinogenesis in mammals, but was also identified as a sensitive indicator of early steps of pollution-induced carcinogenesis in fish (Winzer et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Effect of chronic exposure to sublethal of ammonia concentrations on NADP+-dependent dehydrogenases of Nile tilapia liver

Hegazi¹

2011

Egypt. J. of Aquatic Biolo. and Fish.

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he effect of chronic exposure to sublethal ammonia (NH 3) on liver NADPH producing enzymes of Nile tilapia juveniles (Oreochromis niloticus) was studied. Fish with an initial weight of 15.0±1.4 g were reared in a static system and exposed to the total ammonia nitrogen (TAN) concentrations 5 or 10 mg L −1 for consecutive 70 days at 26±0.5°C. NADPH is mainly produced by glucose 6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase (6PGDH), and the cytosolic form of NADP-dependent isocitrate dehydrogenase (IDH). These enzymes have been recently considered as an important factor in cellular defense against oxidative damage as they share in maintaining reduced glutathione (GSH) level. The activity of the enzymes G6PDH, 6PGDH, and cytosolic IDH in liver tissues of fish exposed to different concentrations of NH 3 showed significant increase. The degree of increase in activity was positively related to ammonia concentration. The increased activity of these enzymes resulted in higher NADPH availability. This may be interpreted as a defense to maintain a high level of GSH against the expected oxidative stress in ammonia-exposed fish.

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“…G6PD is elevated in response to external stimuli (hormones, growth factors, nutrients, and toxic and oxidative stress; Swezey and Epel 1986;Stanton et al 1991;Kletzien et al 1994;Jonges et al 1995;Spolarics 1998;Amir-Ahmady and Salati 2001). G6PD activity is strongly upregulated in proliferating cells, such as malignant cells (Weber 1977;Bannasch et al 1981;Stumpf and Bannasch 1994;Van Driel et al 1997;Kuo et al 2000). There is increasing evidence that G6PD activity is of major importance for NADPH production for defense against oxidative stress (Storz and Altuvia 1994;Pandolfi et al 1995;Izawa et al 1998;Spolarics 1998;Biagiotti et al 2000;Winzer et al 2001) rather than for ribose production during proliferation.…”

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confidence: 99%

Post-translational Regulation of Glucose-6-phosphate Dehydrogenase Activity in (Pre)neoplastic Lesions in Rat Liver

Frederiks

Bosch

Jong

et al. 2003

J Histochem Cytochem.

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S U M M A R Y Glucose-6-phosphate dehydrogenase (G6PD; EC 1.1.1.49) is the key regulatory enzyme of the pentose phosphate pathway and produces NADPH and riboses. In this study, the kinetic properties of G6PD activity were determined in situ in chemically induced hepatocellular carcinomas, and extralesional and control parenchyma in rat livers and were directly compared with those of the second NADPH-producing enzyme of the pentose phosphate pathway, phosphogluconate dehydrogenase (PGD). Distribution patterns of G6PD activity, protein, and mRNA levels were also compared to establish the regulation mechanisms of G6PD activity. In (pre)neoplastic lesions, the V max of G6PD was 150-fold higher and the K m for G6P was 10-fold higher than in control liver parenchyma, whereas in extralesional parenchyma, the V max was similar to that in normal parenchyma but the K m was fivefold lower. This means that virtual fluxes at physiological substrate concentrations are 20-fold higher in lesions and twofold higher in extralesional parenchyma than in normal parenchyma. The V max of PGD was fivefold higher in lesions than in normal and extralesional liver parenchyma, whereas the K m was not affected. Amounts of G6PD protein and mRNA were similar in lesions and in extralesional liver parenchyma. These results demonstrate that G6PD is strongly activated post-translationally in (pre)neoplastic lesions to produce NADPH.

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Overexpression of Glucose-6-Phosphate-Dehydrogenase in Rat Hepatic Preneoplasia and Neoplasia

Cited by 10 publications

References 35 publications

Emerging Role of the Pentose Phosphate Pathway in Hepatocellular Carcinoma

Emerging Role of the Pentose Phosphate Pathway in Hepatocellular Carcinoma

Effect of chronic exposure to sublethal of ammonia concentrations on NADP+-dependent dehydrogenases of Nile tilapia liver

Post-translational Regulation of Glucose-6-phosphate Dehydrogenase Activity in (Pre)neoplastic Lesions in Rat Liver

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