Elevated Expression of Glycerol-3-Phosphate Phosphatase as a Biomarker of Poor Prognosis and Aggressive Prostate Cancer

Lounis, Mohamed Amine; Ouellet, Véronique; Péant, Benjamin; Caron, Christine; Li, Zhenhong; Al‐Mass, Anfal; Mes-Masson, Anne-Marie; Saad, Fred

doi:10.3390/cancers13061273

Cited by 6 publications

(2 citation statements)

References 34 publications

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“…In this study, phosphoglycolic acid (VIP >2, p < 0.05, and AUC = 0.975), a differential metabolite, was decreased in patients with liver cirrhosis and muscle mass loss. Phosphoglycolic acid can be regulated by phosphoglycolate phosphatase, which is a recently identified mammalian enzyme at the intersection of glucose metabolism, lipogenesis, lipolysis, and cellular nutrient-excess detoxification ( 43 , 44 ). The relationship between phosphoglycolate phosphatase activity, liver function, and muscle mass was not clear.…”

Section: Discussionmentioning

confidence: 99%

Differential metabolites in cirrhotic patients with hepatitis B and muscle mass loss

Liu

Han²,

Bi³

et al. 2023

Front. Nutr.

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BackgroundSarcopenia leads to complications (infections, hepatic encephalopathy and ascites) and poor overall survival in patients with cirrhosis, in which the phenotypic presentation is loss of muscle mass. This study aimed to reveal the metabolic profile and identify potential biomarkers in cirrhotic patients with hepatitis B virus and muscle mass loss.MethodTwenty decompensated cirrhotic patients with HBV and muscle mass loss were designated Group S; 20 decompensated cirrhotic patients with HBV and normal muscle mass were designated Group NS; and 20 healthy people were designated Group H. Muscle mass loss was defined as the skeletal muscle mass index less than 46.96 cm2/m2 for males and less than 32.46 cm2/m2 for females. Gas chromatography–mass spectrometry was used to explore the distinct metabolites and pathways in the three groups.ResultsThirty-seven metabolic products and 25 associated metabolic pathways were significantly different in the Group S patients from Group NS patients. Strong predictive value of 11 metabolites (inosine-5′-monophosphate, phosphoglycolic acid, D-fructose-6-phosphate, N-acetylglutamate, pyrophosphate, trehalose-6-phosphate, fumaric acid, citrulline, creatinine, (r)-3-hydroxybutyric acid, and 2-ketobutyric acid) were selected as potential biomarkers in Group S patients compared with Group NS patients. Two pathways may be associated with loss of muscle mass in patients with liver cirrhosis: amino acid metabolism and central carbon metabolism in cancer.ConclusionSeventy differential metabolites were identified in patients who have liver cirrhosis and loss of muscle mass compared with patients who have cirrhosis and normal muscle mass. Certain biomarkers might distinguish between muscle mass loss and normal muscle mass in HBV-related cirrhosis patients.

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Section: Discussionmentioning

confidence: 99%

Differential metabolites in cirrhotic patients with hepatitis B and muscle mass loss

Liu

Han²,

Bi³

et al. 2023

Front. Nutr.

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“…Although never investigated before, it seems that a role in this ambit is very plausible. In fact, it has been recently demonstrated that tumors, primarily dependent on glycolysis to support their elevated growth demands (Warburg effect) [26], like typically mPCa is [27], are able to modulate expression of specific genes relevant to cancer cell immune escape [28]. Of note, Glo1 is an enzyme involved in glucose metabolism due to its capacity of metabolizing MG, a by-product of glycolysis through the intermediates, in particular, from the non-enzymatic degradation of dihydroxyacetone phosphate and glyceraldehyde-3-phosphate [21].…”

Section: Introductionmentioning

confidence: 99%

Glyoxalase-1-Dependent Methylglyoxal Depletion Sustains PD-L1 Expression in Metastatic Prostate Cancer Cells: A Novel Mechanism in Cancer Immunosurveillance Escape and a Potential Novel Target to Overcome PD-L1 Blockade Resistance

Antognelli

Mandarano

Prosperi

et al. 2021

Cancers

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Metastatic prostate cancer (mPCa) is a disease for which to date there is not curative therapy. Even the recent and attractive immunotherapeutic approaches targeting PD-L1, an immune checkpoint protein which helps cancer cells to escape from immunosurveillance, have proved ineffective. A better understanding of the molecular mechanisms contributing to keep an immunosuppressive microenvironment associated with tumor progression and refractoriness to PD-L1 inhibitors is urgently needed. In the present study, by using gene silencing and specific activators or scavengers, we demonstrated, in mPCa cell models, that methylglyoxal (MG), a potent precursor of advanced glycation end products (AGEs), especially 5-hydro-5-methylimidazolone (MG-H1), and its metabolizing enzyme, glyoxalase 1 (Glo1), contribute to maintain an immunosuppressive microenvironment through MG-H1-mediated PD-L1 up-regulation and to promote cancer progression. Moreover, our findings suggest that this novel mechanism might be responsible, at least in part, of mPCa resistance to PD-L1 inhibitors, such as atezolizumab, and that targeting it may sensitize cells to this PD-L1 inhibitor. These findings provide novel insights into the mechanisms of mPCa immunosurveillance escape and help in providing the basis to foster in vivo research toward novel therapeutic strategies for immunotherapy of mPCa.

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From antiepileptic therapy to promising adjuvant in medical oncology: A historical view of the ketogenic diet

2023

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Elevated Expression of Glycerol-3-Phosphate Phosphatase as a Biomarker of Poor Prognosis and Aggressive Prostate Cancer

Cited by 6 publications

References 34 publications

Differential metabolites in cirrhotic patients with hepatitis B and muscle mass loss

Differential metabolites in cirrhotic patients with hepatitis B and muscle mass loss

Glyoxalase-1-Dependent Methylglyoxal Depletion Sustains PD-L1 Expression in Metastatic Prostate Cancer Cells: A Novel Mechanism in Cancer Immunosurveillance Escape and a Potential Novel Target to Overcome PD-L1 Blockade Resistance

From antiepileptic therapy to promising adjuvant in medical oncology: A historical view of the ketogenic diet

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