Metabolic control of the cell cycle

Kalucka, Joanna; Missiaen, Rindert; Γεωργιάδου, Μαρία; Schoors, Sandra; Lange, Christian; Bock, Katrien De; Dewerchin, Mieke; Carmeliet, Peter

doi:10.1080/15384101.2015.1090068

Cited by 87 publications

(71 citation statements)

References 74 publications

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“…Though glycolysis produces only two ATP molecules per molecule of glucose, because it is rapid, it can provide glucose at a faster rate than oxidative phosphorylation . Glycolysis also provides metabolic intermediates . The glycolytic intermediate 3‐phosphoglycerate can be used to generate amino acids; dihydroxyacetone phosphate and acetyl‐CoA can be used for lipid synthesis; glucose‐6‐phosphate can be used to generate nucleotides .…”

Section: Shift In Metabolism With the Transition Between Quiescence Amentioning

confidence: 99%

“…PFKFB3 is an isoform that has a high kinase to phosphatase activity and consequently mostly promotes glycolysis . In human endothelial cells, there is an increase in glycolytic flux prior to cell cycle commitment . Overexpression of the glycolytic enzyme PFKFB3 was sufficient to promote cell cycle entry of endothelial cells , while knockdown of PFKFB3 impairs angiogenesis, thus demonstrating the importance of regulation of glycolytic rate as a determinant of proliferation rate.…”

Section: Molecules That Mediate the Shift To Higher Glycolysis With Pmentioning

confidence: 99%

“…The E2F transcription factor is an important regulator of cell cycle entry , and also serves to coordinate proliferation with metabolism in mammalian cells . One mechanism by which E2F regulates metabolism is by upregulating pyruvate dehydrogenase kinase, an enzyme that phosphorylates and inhibits pyruvate dehydrogenase, the enzyme that converts pyruvate to lactate .…”

Section: Molecules That Mediate the Shift To Higher Glycolysis With Pmentioning

confidence: 99%

“…mTOR activation in proliferating human mammary epithelial cells was found to contribute to the change in glutamine metabolism . Glutamine breakdown, in addition to glucose consumption, is also important to provide energy for cells that are proliferating . Glutamine breakdown is essential for progression to S phase and for progression from S to G2/M phase in HeLa ovarian cancer cells .…”

Section: Amino Acid Metabolismmentioning

confidence: 99%

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The paradox of metabolism in quiescent stem cells

Coller

2019

FEBS Letters

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The shift between a proliferating and a nonproliferating state is associated with significant changes in metabolic needs. Proliferating cells tend to have higher metabolic rates, and their metabolic profiles facilitate biosynthesis, as compared to those of nondividing cells of the same sort. Recent studies have elucidated specific molecules that control metabolic changes while cells shift between proliferation and quiescence. Embryonic stem cells, which are rapidly proliferating, tend to have metabolic patterns that are similar to those of nonstem cells in a proliferative state. Moreover, although adult stem cells tend to be quiescent, their metabolic profiles have been reported in multiple organs to more closely resemble those of proliferating than those of nondividing cells in some respects. The findings raise questions about whether there are metabolic profiles that are required for stemness, and whether these profiles relate to the metabolic properties that may be required for quiescence. Here, we review the literature on how metabolism changes upon commitment to proliferation and compare the proliferating and nonproliferating metabolic states of differentiated cells and embryonic and adult stem cells.

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Section: Shift In Metabolism With the Transition Between Quiescence Amentioning

confidence: 99%

Section: Molecules That Mediate the Shift To Higher Glycolysis With Pmentioning

confidence: 99%

Section: Molecules That Mediate the Shift To Higher Glycolysis With Pmentioning

confidence: 99%

Section: Amino Acid Metabolismmentioning

confidence: 99%

See 2 more Smart Citations

The paradox of metabolism in quiescent stem cells

Coller

2019

FEBS Letters

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“…Addiction of endothelial cells on anaerobic rather than aerobic pathway enables them for the formation of vascular sprouts in hypoxic areas. 97,98 Metabolism of tumor endothelial cells resembles that of highly activated endothelial cells because of the tumor induced switch from quiescence to proliferation due to metabolically regulated migration during sprouting. 99,100 …”

Section: Arginine Deiminasementioning

confidence: 99%

Arginine dependence of tumor cells: targeting a chink in cancer’s armor

et al. 2016

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Arginine, one among the 20 most common natural amino acids, has a pivotal role in cellular physiology as it is being involved in numerous cellular metabolic and signaling pathways. Dependence on arginine is diverse for both tumor and normal cells. Because of decreased expression of argininosuccinate synthetase and/or ornithine transcarbamoylase, several types of tumor are auxotrophic for arginine. Deprivation of arginine exploits a significant vulnerability of these tumor cells and leads to their rapid demise. Hence, enzyme-mediated arginine depletion is a potential strategy for the selective destruction of tumor cells. Arginase, arginine deiminase and arginine decarboxylase are potential enzymes that may be used for arginine deprivation therapy. These arginine catabolizing enzymes not only reduce tumor growth but also make them susceptible to concomitantly administered anti-cancer therapeutics. Most of these enzymes are currently under clinical investigations and if successful will potentially be advanced as anti-cancer modalities.

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Multiomics integrative analysis reveals antagonistic roles of CBX2 and CBX7 in metabolic reprogramming of breast cancer

et al. 2021

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Striking similarity exists between metabolic changes associated with embryogenesis and tumorigenesis. Chromobox proteins‐CBX2/4/6/7/8, core components of canonical polycomb repressor complex 1, play essential roles in embryonic development and aberrantly expressed in breast cancer. Understanding how altered CBX expression relates to metabolic reprogramming in breast cancer may reveal vulnerabilities of therapeutic pertinence. Using transcriptomic and metabolomic data from breast cancer patients ( N > 3000 combined), we performed pathway‐based analysis and identified outstanding roles of CBX2 and CBX7 in positive and negative regulation of glucose metabolism, respectively. Genetic ablation experiments validated the contrasting roles of two isoforms in cancer metabolism and cell growth. Furthermore, we provide evidence for the role of mammalian target of rapamycin complex 1 signaling in mediating contrary effects of CBX2 and CBX7 on breast cancer metabolism. Underpinning the biological significance of metabolic roles, CBX2 and CBX7 were found to be the most up‐ and downregulated isoforms, respectively, in breast tumors compared with normal tissues. Moreover, CBX2 and CBX7 expression (not other isoforms) correlated strongly, but oppositely, with breast tumor subtype aggressiveness and the proliferation markers. Consistently, genomic data also showed higher amplification frequency of CBX2, not CBX7, in breast tumors. Highlighting the clinical significance of findings, disease‐specific survival and drug sensitivity analysis revealed that CBX2 and CBX7 predicted patient outcome and sensitivity to FDA‐approved/investigational drugs. In summary, this work identifies novel cross talk between CBX2/7 and breast tumor metabolism, and the results presented may have implications in strategies targeting breast cancer.

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Metabolic control of the cell cycle

Cited by 87 publications

References 74 publications

The paradox of metabolism in quiescent stem cells

The paradox of metabolism in quiescent stem cells

Arginine dependence of tumor cells: targeting a chink in cancer’s armor

Multiomics integrative analysis reveals antagonistic roles of CBX2 and CBX7 in metabolic reprogramming of breast cancer

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