Expression of hypoxia‐inducible factor 1α, glucose transporter 1, and hexokinase 2 in primary central nervous system lymphoma and the correlation with the biological behaviors

Shen, Na; Wang, Yaming; Sun, Xin; Bai, Xueyan; He, Jinglan; Cui, Qu; Qian, Jun; Zhu, Hong; Chen, Yuedan; Xing, Ruixian; Liu, Qing; Wu, Yuchen; Li, Junhong; Lai, Wenyuan; Sun, Shilong; Ji, Nan; Liu, Yuanbo

doi:10.1002/brb3.1718

Cited by 11 publications

(4 citation statements)

References 34 publications

(36 reference statements)

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“…Persistent hypoxia can additionally enhance local and systemic malignant progression and may also extend increase invasiveness through the clonal selection and genomic and proteomic changes (Dachs and Chaplin, 1998). HIF-1α is a major regulator of glycolysis (Shen et al, 2020). Under hypoxia, HIF-1α plays an important role in the transcription of genes involved in angiogenesis, tumor growth, invasion, metastasis, and glucose metabolism (Soni and Padwad, 2017).…”

Section: Discussionmentioning

confidence: 99%

Expression and Clinical Significance of HKII and HIF-1α in Grade Groups of Prostate Cancer

et al. 2021

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Prostate cancer (PCA) is the second leading cause of cancer-related mortality in men. The glycolytic enzymes hexokinase II (HKII) and the major regulator hypoxia-inducible factor-1α (HIF-1α) are PCA-specific biomarkers. Some studies have shown that HKII and HIF-1α are highly expressive in PCA and are associated with the growth and metastasis of treatment. Whether HKII and HIF-1α regulate the different differentiation of PCA remains largely unknown. Therefore, the study aims to explore the value of HKII and HIF-1α in different grade groups of PCA. Our data indicated that compared with normal prostate tissues, the level of mRNA and protein of HKII and HIF-1α in PCA increased significantly, besides the results showed the high expression of HKII and HIF-1α had a tendency to promote the progression and differentiation of PCA. The study also found that HKII expression was positively correlated with the expression of HIF-1α. HKII and HIF-1α were related to the degree of differentiation PCA, especially in high-grade PCA. Furthermore, the high expression of HKII was significantly associated with Gleason score and histological differentiation in clinicopathological characteristics of patients with PCA. These results were further used to confirm that the expression of HKII and HIF-1α was associated with the progression and differentiation of PCA. These experiments indicated that HKII and HIF-1α might be novel biomarkers of PCA with potential clinical application value, provide a new potential target for PCA treatment, and are expected to be used for individualized treatment in patients with PCA.

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Section: Discussionmentioning

confidence: 99%

Expression and Clinical Significance of HKII and HIF-1α in Grade Groups of Prostate Cancer

et al. 2021

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“…HIF-1α is an important transcription factor that regulates glucose uptake and glycolysis at the transcriptional level (Huang et al, 2012 ; Harris et al, 2014 ; Masoud and Li, 2015 ). Several studies have shown that HIF-1α upregulates glucose transporters (GLUT1, GLUT3, GLUT4; Toberer et al, 2020 ), glycolysis enzyme (HK2; Cao et al, 2020 ; Shen et al, 2020 ), pro-angiogenic factors (HO-1, VEGF; Choi et al, 2006 ). Whereas, downregulation of HIF-1α suppressed the target genes and protein expressions, such as GLUT1, GLUT3, and HK2 (Liu et al, 2008 ; Lee et al, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

α-Lipoic Acid Maintains Brain Glucose Metabolism via BDNF/TrkB/HIF-1α Signaling Pathway in P301S Mice

Zhang

Yan

et al. 2020

Front. Aging Neurosci.

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The microtubule-associated protein tau is closely correlated with hypometabolism in Alzheimer's disease (AD). α-lipoic acid (LA), which is a naturally occurring cofactor in mitochondrial, has been shown to have properties that can inhibit the tau pathology and neuronal damage in our previous research. However, if LA affects glucose metabolism when it reverses tau pathology remains unclear, especially concerning the potential mechanism. Therefore, we make a further study using the P301S mouse model (a tauopathy and AD mouse model which overexpressing fibrillary tau) to gain a clear idea of the aforementioned problems. Here, we found chronic LA administration significantly increased glucose availability by elevating glucose transporter 3 (GLUT3), GLUT4, vascular endothelial growth factor (VEGF) protein and mRNA level, and heme oxygenase-1 (HO-1) protein level in P301S mouse brains. Meanwhile, we found that LA also promoted glycolysis by directly upregulating hexokinase (HK) activity, indirectly by increasing proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and DNA repair enzymes (OGG1/2 and MTH1). Further, we found the underlying mechanism of restored glucose metabolism might involve in the activation of brain-derived neurotrophic factor (BDNF)/tyrosine Kinase receptor B (TrkB)/hypoxia-inducible factor-1α (HIF-1α) signaling pathway by LA treatment.

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“…In comparison to mitochondria, O 2 •- produced by NOX is dismutated into H 2 O 2 by superoxide dismutase1 (SOD1), whereas nitric oxide produced by inducible nitric oxide synthase (iNOS) reacts with O 2 •- resulting in peroxynitrite production ( 19 ). For example, ROS drive hypoxia-inducible factor 1α (HIF1α) mediated GLUT1 expression, hexokinase activity, and resultant glycolysis in response to low oxygen tension as part of the angiogenic response ( 27 ) The co-localization of neutrophil phosphofructokinase 2 with NOX2 leads to its activation, resulting in NADP+ production as its byproduct, facilitating an enhanced glycolytic rate. The increase in glycolysis rate and enhancement of NOX2 activity and the relation between these processes are still under study ( 28 ).…”

Section: Ros In Sensing and Reaction To Damagementioning

confidence: 99%

ROS signaling in innate immunity via oxidative protein modifications

Manoharan,

Prasad,

Pospíšil

et al. 2024

Front. Immunol.

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The innate immune response represents the first-line of defense against invading pathogens. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) have been implicated in various aspects of innate immune function, which involves respiratory bursts and inflammasome activation. These reactive species widely distributed within the cellular environment are short-lived intermediates that play a vital role in cellular signaling and proliferation and are likely to depend on their subcellular site of formation. NADPH oxidase complex of phagocytes is known to generate superoxide anion radical (O2•−) that functions as a precursor for antimicrobial hydrogen peroxide (H2O2) production, and H2O2 is utilized by myeloperoxidase (MPO) to generate hypochlorous acid (HOCl) that mediates pathogen killing. H2O2 modulates the expression of redox-responsive transcriptional factors, namely NF-kB, NRF2, and HIF-1, thereby mediating redox-based epigenetic modification. Survival and function of immune cells are under redox control and depend on intracellular and extracellular levels of ROS/RNS. The current review focuses on redox factors involved in the activation of immune response and the role of ROS in oxidative modification of proteins in macrophage polarization and neutrophil function.

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Expression of hypoxia‐inducible factor 1α, glucose transporter 1, and hexokinase 2 in primary central nervous system lymphoma and the correlation with the biological behaviors

Cited by 11 publications

References 34 publications

Expression and Clinical Significance of HKII and HIF-1α in Grade Groups of Prostate Cancer

Expression and Clinical Significance of HKII and HIF-1α in Grade Groups of Prostate Cancer

α-Lipoic Acid Maintains Brain Glucose Metabolism via BDNF/TrkB/HIF-1α Signaling Pathway in P301S Mice

ROS signaling in innate immunity via oxidative protein modifications

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