Digging deeper through glucose metabolism and its regulators in cancer and metastasis

Ghanavat, Majid; Shahrouzian, Mehdi; Zayeri, Zeinab Deris; Banihashemi, Sara; Kazemi, S Maryam; Saki, Najmaldin

doi:10.1016/j.lfs.2020.118603

Cited by 63 publications

(53 citation statements)

References 208 publications

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“…The high output of lactate also generates an acidic microenvironment where only cells with phenotypes resistant to acidic environments can grow. This offers a huge growth advantage and intensifies the invasive and metastatic nature of cancer cells, as other cells around them deteriorate [ 6 ].…”

Section: Glucose Metabolism and The Warburg Effect: A Century Latermentioning

confidence: 99%

Mechanisms of Metabolic Reprogramming in Cancer Cells Supporting Enhanced Growth and Proliferation

Schiliro

Firestein

2021

Cells

276

152

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Cancer cells alter metabolic processes to sustain their characteristic uncontrolled growth and proliferation. These metabolic alterations include (1) a shift from oxidative phosphorylation to aerobic glycolysis to support the increased need for ATP, (2) increased glutaminolysis for NADPH regeneration, (3) altered flux through the pentose phosphate pathway and the tricarboxylic acid cycle for macromolecule generation, (4) increased lipid uptake, lipogenesis, and cholesterol synthesis, (5) upregulation of one-carbon metabolism for the production of ATP, NADH/NADPH, nucleotides, and glutathione, (6) altered amino acid metabolism, (7) metabolism-based regulation of apoptosis, and (8) the utilization of alternative substrates, such as lactate and acetate. Altered metabolic flux in cancer is controlled by tumor-host cell interactions, key oncogenes, tumor suppressors, and other regulatory molecules, including non-coding RNAs. Changes to metabolic pathways in cancer are dynamic, exhibit plasticity, and are often dependent on the type of tumor and the tumor microenvironment, leading in a shift of thought from the Warburg Effect and the “reverse Warburg Effect” to metabolic plasticity. Understanding the complex nature of altered flux through these multiple pathways in cancer cells can support the development of new therapies.

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Section: Glucose Metabolism and The Warburg Effect: A Century Latermentioning

confidence: 99%

Mechanisms of Metabolic Reprogramming in Cancer Cells Supporting Enhanced Growth and Proliferation

Schiliro

Firestein

2021

Cells

276

152

View full text Add to dashboard Cite

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“…Specifically, cancer cells exhibit metabolic reprogramming such as dysregulated glucose uptake, excessive lipid synthesis and glutaminolysis [110]. These transformations are essential parameters in the maintenance and development of malignant phenotypes in harsh microenvironments [111][112][113][114][115]. The role of IGF2BP2 in glucose tolerance, insulin sensitivity, fatty acid oxidation and the development of metabolic diseases had been reviewed recently [13, 21-23, 28, 53].…”

Section: Discussionmentioning

confidence: 99%

The role of IGF2BP2, an m6A reader gene, in human metabolic diseases and cancers

2021

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The human insulin-like growth factor 2 (IGF2) mRNA binding proteins 2 (IGF2BP2/IMP2) is an RNA-binding protein that regulates multiple biological processes. Previously, IGF2BP2 was thought to be a type 2 diabetes (T2D)-associated gene. Indeed IGF2BP2 modulates cellular metabolism in human metabolic diseases such as diabetes, obesity and fatty liver through post-transcriptional regulation of numerous genes in multiple cell types. Emerging evidence shows that IGF2BP2 is an N6-methyladenosine (m6A) reader that participates in the development and progression of cancers by communicating with different RNAs such as microRNAs (miRNAs), messenger RNAs (mRNAs) and long non-coding RNAs (lncRNAs). Additionally, IGF2BP2 is an independent prognostic factor for multiple cancer types. In this review, we summarize the current knowledge on IGF2BP2 with regard to diverse human metabolic diseases and its potential for cancer prognosis.

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“…glucose uptake by inducing GLUT expression. In addition, the PI3K/Akt/mTOR pathway induces glycolytic enzymes and GLUT expression, and p53 regulates glycolysis and GLUT through mTOR and AMP-activated protein kinase (AMPK) (Abdel-Wahab et al, 2019;Ghanavat et al, 2021).…”

Section: General Aspects Of Glucose Metabolism and Related Metabolic Pathways In Cancermentioning

confidence: 99%

“…Oncogenes such as Ras, Src, and MYC increase the expression of HIF-1 that increases the expression of various glycolytic enzymes, and HIF-1, MYC, and KRAS increase glucose uptake by inducing GLUT expression. In addition, the PI3K/Akt/mTOR pathway induces glycolytic enzymes and GLUT expression, and p53 regulates glycolysis and GLUT through mTOR and AMP-activated protein kinase (AMPK) ( Abdel-Wahab et al, 2019 ; Ghanavat et al, 2021 ).…”

Section: General Aspects Of Glucose Metabolism and Related Metabolic Pathways In Cancermentioning

confidence: 99%

Glucose Metabolism and Glucose Transporters in Breast Cancer

Shin

Koo

2021

Front. Cell Dev. Biol.

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Breast cancer is the most common malignancy in women worldwide and is associated with high mortality rates despite the continuously advancing treatment strategies. Glucose is essential for cancer cell metabolism owing to the Warburg effect. During the process of glucose metabolism, various glycolytic metabolites, such as serine and glycine metabolites, are produced and other metabolic pathways, such as the pentose phosphate pathway (PPP), are associated with the process. Glucose is transported into the cell by glucose transporters, such as GLUT. Breast cancer shows high expressions of glucose metabolism-related enzymes and GLUT, which are also related to breast cancer prognosis. Triple negative breast cancer (TNBC), which is a high-grade breast cancer, is especially dependent on glucose metabolism. Breast cancer also harbors various stromal cells such as cancer-associated fibroblasts and immune cells as tumor microenvironment, and there exists a metabolic interaction between these stromal cells and breast cancer cells as explained by the reverse Warburg effect. Breast cancer is heterogeneous, and, consequently, its metabolic status is also diverse, which is especially affected by the molecular subtype, progression stage, and metastatic site. In this review, we will focus on glucose metabolism and glucose transporters in breast cancer, and we will additionally discuss their potential applications as cancer imaging tracers and treatment targets.

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Digging deeper through glucose metabolism and its regulators in cancer and metastasis

Cited by 63 publications

References 208 publications

Mechanisms of Metabolic Reprogramming in Cancer Cells Supporting Enhanced Growth and Proliferation

Mechanisms of Metabolic Reprogramming in Cancer Cells Supporting Enhanced Growth and Proliferation

The role of IGF2BP2, an m6A reader gene, in human metabolic diseases and cancers

Glucose Metabolism and Glucose Transporters in Breast Cancer

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