A short review on cross-link between pyruvate kinase (PKM2) and Glioblastoma Multiforme

Verma, Harkomal; Cholia, Ravi P.; Kaur, Sharanjot; Dhiman, Monisha; Mantha, Anil K.

doi:10.1007/s11011-021-00690-y

Cited by 21 publications

(11 citation statements)

References 111 publications

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“…Finally, overexpression of pyruvate kinase M1/2 is a trait occurring in brain tumors but not in other cancers, where it is involved in metabolic and signaling functions that promote cell proliferation, migration and chemoresistance. Knocking down PKM alters central carbon metabolism and decreases the activation of oncogenes, thus making it a viable therapy target 66 .…”

Section: Resultsmentioning

confidence: 99%

Metabolic modeling-based drug repurposing in Glioblastoma

Tomi-Andrino

Pandele

Winzer

et al. 2022

Sci Rep

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The manifestation of intra- and inter-tumor heterogeneity hinders the development of ubiquitous cancer treatments, thus requiring a tailored therapy for each cancer type. Specifically, the reprogramming of cellular metabolism has been identified as a source of potential drug targets. Drug discovery is a long and resource-demanding process aiming at identifying and testing compounds early in the drug development pipeline. While drug repurposing efforts (i.e., inspecting readily available approved drugs) can be supported by a mechanistic rationale, strategies to further reduce and prioritize the list of potential candidates are still needed to facilitate feasible studies. Although a variety of ‘omics’ data are widely gathered, a standard integration method with modeling approaches is lacking. For instance, flux balance analysis is a metabolic modeling technique that mainly relies on the stoichiometry of the metabolic network. However, exploring the network’s topology typically neglects biologically relevant information. Here we introduce Transcriptomics-Informed Stoichiometric Modelling And Network analysis (TISMAN) in a recombinant innovation manner, allowing identification and validation of genes as targets for drug repurposing using glioblastoma as an exemplar.

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Section: Resultsmentioning

confidence: 99%

Metabolic modeling-based drug repurposing in Glioblastoma

Tomi-Andrino

Pandele

Winzer

et al. 2022

Sci Rep

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“…PK catalyzes the conversion of phosphoenolpyruvate (PEP) to pyruvate, which is the final step of glycolysis. PK has four isoforms: PKL (liver), PKR (erythrocytes), PKM1 (muscle and brain), and PKM2 (brain and liver) [ 141 , 142 , 143 ]. PKM2 can be a tetramer or dimer and the tetrameric form has a higher affinity for PEP, while the dimer has a lower affinity.…”

Section: Glycolysis and Autophagy Regulation In Cancermentioning

confidence: 99%

Regulation of Autophagy via Carbohydrate and Lipid Metabolism in Cancer

Alizadeh

Kavoosi

Singh

et al. 2023

Cancers

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Metabolic changes are an important component of tumor cell progression. Tumor cells adapt to environmental stresses via changes to carbohydrate and lipid metabolism. Autophagy, a physiological process in mammalian cells that digests damaged organelles and misfolded proteins via lysosomal degradation, is closely associated with metabolism in mammalian cells, acting as a meter of cellular ATP levels. In this review, we discuss the changes in glycolytic and lipid biosynthetic pathways in mammalian cells and their impact on carcinogenesis via the autophagy pathway. In addition, we discuss the impact of these metabolic pathways on autophagy in lung cancer.

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“…PK catalyzes the conversion of phosphoenolpyruvate (PEP) to pyruvate, which is the final step of glycolysis. PK has four isoforms: PKL (liver), PKR (erythrocytes), PKM1 (muscle and brain), and PKM2 (brain and liver) [137][138][139]. PKM2 can be a tetramer or dimer and the tetramer form has a higher affinity for PEP, while the dimer has lower affinity.…”

Section: Pyruvate Kinase (Pk)mentioning

confidence: 99%

Regulation of Autophagy via Carbohydrate and Lipid Metabolism in Cancer

Alizadeh¹,

Kavoosi²,

Singh³

et al. 2023

Preprint

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Metabolic changes are an important component of tumor cell progression. Tumor cells adapt to environmental stresses via changes to carbohydrate and lipid metabolism. Autophagy, a physiological process in mammalian cells that digests damaged organelles and misfolded proteins via lysosomal degradation is closely associated with metabolism in mammalian cells acting as a meter of cellular ATP levels. In this review, we discuss the changes in glycolytic and lipid biosynthetic pathways in mammalian cells and their impact on carcinogenesis via the autophagy pathway. Also, we discuss the impact of these metabolic pathways on autophagy in lung cancer.

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A short review on cross-link between pyruvate kinase (PKM2) and Glioblastoma Multiforme

Cited by 21 publications

References 111 publications

Metabolic modeling-based drug repurposing in Glioblastoma

Metabolic modeling-based drug repurposing in Glioblastoma

Regulation of Autophagy via Carbohydrate and Lipid Metabolism in Cancer

Regulation of Autophagy via Carbohydrate and Lipid Metabolism in Cancer

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