IDH2, a novel target of OGT, facilitates glucose uptake and cellular bioenergy production via NF-κB signaling to promote colorectal cancer progression

He, Xiaoli; Wu, Nan; Li, Renlong; Zhang, Haohao; Zhao, Yu; Nie, Yongzhan; Jing, Wu

doi:10.1007/s13402-022-00740-2

Cited by 14 publications

(5 citation statements)

References 64 publications

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“…In the TCA cycle, the mutation of IDH1/2 can also cause inconsistent changes in some metabolic intermediates, such as 2-OG, citrate, cis-aconite, isocitrate, and fumarate [ 245 , 249 , 250 , 251 , 252 , 253 , 254 ]. However, compared with WT–IDH cells that are dominated by glycolysis [ 255 , 256 ], IDH mutant tumour cells have a stronger TCA cycle [ 256 , 257 , 258 ], more OXPHOS [ 259 ], and lower glycolysis levels [ 256 , 260 , 261 ]. This may be related to using different carbon sources after the IDH mutation.…”

Section: Molecules Affecting Tumour Glycolysis and Oxphos Transformat...mentioning

confidence: 99%

“…In addition to the above examples, compared with mutant IDH tumour cells, wild-type IDH has higher levels of glycolysis and TCA [ 255 , 276 ], which mainly depends on glucose and glutamine metabolism to generate pyruvate and α-KG [ 248 , 277 , 278 ]. Moreover, the survival rate of patients with wild-type IDH tumours is not as good as that of IDH mutant patients [ 279 , 280 ], which may be related to the different responses of these tumour patients to IDH inhibitors [ 267 ].…”

Section: Molecules Affecting Tumour Glycolysis and Oxphos Transformat...mentioning

confidence: 99%

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Regulative Roles of Metabolic Plasticity Caused by Mitochondrial Oxidative Phosphorylation and Glycolysis on the Initiation and Progression of Tumorigenesis

Niu

et al. 2023

IJMS

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One important feature of tumour development is the regulatory role of metabolic plasticity in maintaining the balance of mitochondrial oxidative phosphorylation and glycolysis in cancer cells. In recent years, the transition and/or function of metabolic phenotypes between mitochondrial oxidative phosphorylation and glycolysis in tumour cells have been extensively studied. In this review, we aimed to elucidate the characteristics of metabolic plasticity (emphasizing their effects, such as immune escape, angiogenesis migration, invasiveness, heterogeneity, adhesion, and phenotypic properties of cancers, among others) on tumour progression, including the initiation and progression phases. Thus, this article provides an overall understanding of the influence of abnormal metabolic remodeling on malignant proliferation and pathophysiological changes in carcinoma.

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Section: Molecules Affecting Tumour Glycolysis and Oxphos Transformat...mentioning

confidence: 99%

Section: Molecules Affecting Tumour Glycolysis and Oxphos Transformat...mentioning

confidence: 99%

Regulative Roles of Metabolic Plasticity Caused by Mitochondrial Oxidative Phosphorylation and Glycolysis on the Initiation and Progression of Tumorigenesis

Niu

et al. 2023

IJMS

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“…Prior research has indicated that O-GlcNAcylation is a significant factor in determining the relationship between proteins and their E3 ligases [ 38 , 39 ]. Therefore, We focused our attention on whether O-GlcNAcylation modifications are present in TFRC.…”

Section: Resultsmentioning

confidence: 99%

O-GlcNAcylation regulates the stability of transferrin receptor (TFRC) to control the ferroptosis in hepatocellular carcinoma cells

Zhou,

Wang,

et al. 2024

Redox Biology

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“…The overexpression of isocitrate dehydrogenase 2 (IDH2) significantly increased glycolysis and TCA cycle metabolites. O-GlcNAcylation enhanced the protein half-time of IDH2 by inhibiting ubiquitin-mediated proteasome degradation [119].…”

Section: Mitochondrial Energy Metabolismmentioning

confidence: 99%

Roles of O-GlcNAcylation in Mitochondrial Homeostasis and Cardiovascular Diseases

Qiu,

Cui,

Huang

et al. 2024

Antioxidants

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Protein posttranslational modifications are important factors that mediate the fine regulation of signaling molecules. O-linked β-N-acetylglucosamine-modification (O-GlcNAcylation) is a monosaccharide modification on N-acetylglucosamine linked to the hydroxyl terminus of serine and threonine of proteins. O-GlcNAcylation is responsive to cellular stress as a reversible and posttranslational modification of nuclear, mitochondrial and cytoplasmic proteins. Mitochondrial proteins are the main targets of O-GlcNAcylation and O-GlcNAcylation is a key regulator of mitochondrial homeostasis by directly regulating the mitochondrial proteome or protein activity and function. Disruption of O-GlcNAcylation is closely related to mitochondrial dysfunction. More importantly, the O-GlcNAcylation of cardiac proteins has been proven to be protective or harmful to cardiac function. Mitochondrial homeostasis is crucial for cardiac contractile function and myocardial cell metabolism, and the imbalance of mitochondrial homeostasis plays a crucial role in the pathogenesis of cardiovascular diseases (CVDs). In this review, we will focus on the interactions between protein O-GlcNAcylation and mitochondrial homeostasis and provide insights on the role of mitochondrial protein O-GlcNAcylation in CVDs.

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IDH2, a novel target of OGT, facilitates glucose uptake and cellular bioenergy production via NF-κB signaling to promote colorectal cancer progression

Cited by 14 publications

References 64 publications

Regulative Roles of Metabolic Plasticity Caused by Mitochondrial Oxidative Phosphorylation and Glycolysis on the Initiation and Progression of Tumorigenesis

Regulative Roles of Metabolic Plasticity Caused by Mitochondrial Oxidative Phosphorylation and Glycolysis on the Initiation and Progression of Tumorigenesis

O-GlcNAcylation regulates the stability of transferrin receptor (TFRC) to control the ferroptosis in hepatocellular carcinoma cells

Roles of O-GlcNAcylation in Mitochondrial Homeostasis and Cardiovascular Diseases

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