Hyperglycemia, tumorigenesis, and chronic inflammation

Chang, Suying; Yang, Wei

doi:10.1016/j.critrevonc.2016.11.003

Cited by 137 publications

(111 citation statements)

References 97 publications

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“…Consistently, we found that S1P/S1PR3 is activated in both patients with T1D and STZ‐induced diabetic mice, which further demonstrates the important role of S1P/S1PR3 in T1D. DM is characterized by hyperglycemia and has been shown to trigger chronic inflammation . Overwhelming epidemiological and clinical data have demonstrated that patients with DM are more sensitive to IRI .…”

Section: Discussionsupporting

confidence: 81%

“…DM is characterized by hyperglycemia and has been shown to trigger chronic inf lammation. (27) Overwhelming epidemiological and clinical data have demonstrated that patients with DM are more sensitive to IRI. (28) Diabetes and its associated hyperglycemia are involved in a variety of ischemic tissue injuries, including in the lungs, brain, kidney, and liver.…”

Section: Discussionmentioning

confidence: 99%

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Hyperglycemia‐Triggered Sphingosine‐1‐Phosphate and Sphingosine‐1‐Phosphate Receptor 3 Signaling Worsens Liver Ischemia/Reperfusion Injury by Regulating M1/M2 Polarization

Yang

Shen

et al. 2019

Liver Transpl

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Hyperglycemia aggravates hepatic ischemia/reperfusion injury (IRI), but the underlying mechanism for the aggravation remains elusive. Sphingosine‐1‐phosphate (S1P) and sphingosine‐1‐phosphate receptors (S1PRs) have been implicated in metabolic and inflammatory diseases. Here, we discuss whether and how S1P/S1PRs are involved in hyperglycemia‐related liver IRI. For our in vivo experiment, we enrolled diabetic patients with benign hepatic disease who had liver resection, and we used streptozotocin (STZ)–induced hyperglycemic mice or normal mice to establish a liver IRI model. In vitro bone marrow–derived macrophages (BMDMs) were differentiated in high‐glucose (HG; 30 mM) or low‐glucose (LG; 5 mM) conditions for 7 days. The expression of S1P/S1PRs was analyzed in the liver and BMDMs. We investigated the functional and molecular mechanisms by which S1P/S1PRs may influence hyperglycemia‐related liver IRI. S1P levels were higher in liver tissues from patients with diabetes mellitus and mice with STZ‐induced diabetes. S1PR3, but not S1PR1 or S1PR2, was activated in liver tissues and Kupffer cells under hyperglycemic conditions. The S1PR3 antagonist CAY10444 attenuated hyperglycemia‐related liver IRI based on hepatic biochemistry, histology, and inflammatory responses. Diabetic livers expressed higher levels of M1 markers but lower levels of M2 markers at baseline and after ischemia/reperfusion. Dual‐immunofluorescence staining showed that hyperglycemia promoted M1 (CD68/CD86) differentiation and inhibited M2 (CD68/CD206) differentiation. Importantly, CAY10444 reversed hyperglycemia‐modulated M1/M2 polarization. HG concentrations in vitro also triggered S1P/S1PR3 signaling, promoted M1 polarization, inhibited M2 polarization, and enhanced inflammatory responses compared with LG concentrations in BMDMs. In contrast, S1PR3 knockdown significantly retrieved hyperglycemia‐modulated M1/M2 polarization and attenuated inflammation. In conclusion, our study reveals that hyperglycemia specifically triggers S1P/S1PR3 signaling and exacerbates liver IRI by facilitating M1 polarization and inhibiting M2 polarization, which may represent an effective therapeutic strategy for liver IRI in diabetes.

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Section: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Hyperglycemia‐Triggered Sphingosine‐1‐Phosphate and Sphingosine‐1‐Phosphate Receptor 3 Signaling Worsens Liver Ischemia/Reperfusion Injury by Regulating M1/M2 Polarization

Yang

Shen

et al. 2019

Liver Transpl

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“…76,77 In agreement with the in vivo results (Figure 5a), exaggerated elevation of secreted TNF-α was observed in GO-treated cells, relative to untreated cells (Figure 9a, Po0.001), and this elevation was diminished by 27% in cells treated with MoS 2 /GO, compared to GO-treated cells (Figure 9a, Po0.001). In support of this finding, similar results were found for interleukin-6 production ( Figure 9b).…”

Section: Preferential Lung Accumulation Of Mos 2 /Go Nanocompositessupporting

confidence: 77%

Molybdenum disulfide/graphene oxide nanocomposites show favorable lung targeting and enhanced drug loading/tumor-killing efficacy with improved biocompatibility

et al. 2018

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Selective targeting plus optimal biocompatibility is still a big challenge in nanomedicine. Although many nanomaterials including graphene oxide (GO) and molybdenum disulfide (MoS 2 ) have been tested for this purpose, these materials possess both favorable features and drawbacks, which hampers their further development. Herein, we prepared MoS 2 /GO nanocomposites that manifested excellent dispersity in aqueous solutions and revealed acceptable biocompatibility in vitro and in vivo. Importantly, MoS 2 /GO displayed a novel feature to selectively target the lung. In other words, MoS 2 /GO manifested a pronounced tendency of localization towards the lung comparable to GO, offering a 'guided missile' effect in targeting the lung. Furthermore, MoS 2 /GO composites possessed enhanced drug loading capacity together with reinforced tumor-killing efficacy against cancer cells that have the propensity to metastasize to the lung. Importantly, MoS 2 /GO composites remarkably repressed metastatic tumor growth of B16 murine melanoma cancer cells in lungs of mice. Mechanistically, MoS 2 /GO was demonstrated to reveal compromised reactions towards macrophages at the nano-bio interface relative to GO, which is accountable for the interaction and the uptake of nanosheets by macrophages associated with phagocytosis and macrophagic activation. Considered together, our findings established new MoS 2 /GO nanocomposites with multi-functionalities including selective lung targeting, favorable drug loading capacity, elevated tumor killing efficacy and improved biocompatibility. Our study opens an avenue for MoS 2 /GO nanocomposites in cancer nanotheranostics.

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“…We found significantly increased plasma glucose level in all types of primary brain tumours except MNG relative to controls (Table ). In relation to cancer, hyperglycaemia is unfavourable in many aspects, for example, increased blood glucose level increases the risk of cancer, hyperglycaemia is considered as a risk factor for cancer progression, and can also confer resistance and intolerance to chemotherapy …”

Section: Discussionmentioning

confidence: 99%

Metabolomic profiling of blood plasma in patients with primary brain tumours: Basal plasma metabolites correlated with tumour grade and plasma biomarker analysis predicts feasibility of the successful statistical discrimination from healthy subjects – a preliminary study

Baranovičová

Galanda

et al. 2019

IUBMB Life

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The brain tumours represent a complex tissue that has its own characteristic metabolic features and is interfaced with the whole organism. We investigated changes in basal blood plasma metabolites in the presence of primary brain tumour, their correlation with tumour grade, as well as the feasibility of statistical discrimination based on plasma metabolites. Together 60 plasma samples from patients with clinically defined glioblastoma, meningioma, oligodendrioglioma, astrocytoma, and non-specific glial tumour and plasma samples from 28 healthy volunteers without any cancer history were measured by NMR spectroscopy. In blood plasma of primary brain tumour patients, we found significantly increased levels of glycolytic metabolites glucose and pyruvate, and significantly decreased level of glutamine and also metabolites participating in tricarboxylic acid (TCA) cycle, citrate and succinate, when compared with controls. Further, plasma metabolites levels: tyrosine, phenylalanine, glucose, creatine and creatinine correlated significantly with tumour grade. In general, observed changes are parallel to the biochemistry expected for tumourous tissue and metabolic changes in plasma seem to follow the similar rules in all primary brain tumours, with very subtle variations among tumour types. Only two plasma metabolites tyrosine and phenylalanine were increased exclusively in

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Hyperglycemia, tumorigenesis, and chronic inflammation

Cited by 137 publications

References 97 publications

Hyperglycemia‐Triggered Sphingosine‐1‐Phosphate and Sphingosine‐1‐Phosphate Receptor 3 Signaling Worsens Liver Ischemia/Reperfusion Injury by Regulating M1/M2 Polarization

Hyperglycemia‐Triggered Sphingosine‐1‐Phosphate and Sphingosine‐1‐Phosphate Receptor 3 Signaling Worsens Liver Ischemia/Reperfusion Injury by Regulating M1/M2 Polarization

Molybdenum disulfide/graphene oxide nanocomposites show favorable lung targeting and enhanced drug loading/tumor-killing efficacy with improved biocompatibility

Metabolomic profiling of blood plasma in patients with primary brain tumours: Basal plasma metabolites correlated with tumour grade and plasma biomarker analysis predicts feasibility of the successful statistical discrimination from healthy subjects – a preliminary study

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