Control of cellular proliferation by modulation of oxidative phosphorylation in human and rodent fast-growing tumor cells

Rodrı́guez-Enrı́quez, Sara; Vital-González, Paola A.; Flores-Rodríguez, Fanny L.; Marín‐Hernández, Álvaro; Ruíz-Azuara, Lena; Moreno‐Sánchez, Rafael

doi:10.1016/j.taap.2006.02.005

Cited by 101 publications

(81 citation statements)

References 52 publications

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“…For instance, breast cancer cells obtain their energy mainly from mitochondria [38], and this seems to be the case for other epithelial cancers as well, for which the activity of cytochrome oxidase (complex IV) is up-regulated causing a hyperactivation of mitochondrial metabolism [39]. A similar feature has been observed in liver and brain cancer, where a fully functional oxidative phosphorylation has been characterized [40,41]. Mitochondrial oxidative metabolism probably prevails in brain tumors in vivo, as it has been demonstrated that glioblastomas display a preference for glucose oxidation when implanted in mouse brain [42].…”

Section: The Existence Of Functional Mitochondria In Cancer?mentioning

confidence: 71%

Anaplerosis in cancer: Another step beyond the warburg effect

Ochoa-Ruiz¹,

Díaz-Ruiz²

2012

AJMB

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Biosynthesis is up-regulated in tumors and thus the demand for anabolic intermediates is increased. The metabolic routes providing the building blocks for macromolecules are thus a very attractive target as they are not normally up-regulated in a normal quiescent cell. Some routes for glycolysis-derived intermediates production have been identified, but these do not constitute the whole pool of biosynthetic molecules in the cell, as many of these derive from mitochondria in the Krebs cycle. Indeed, this metabolic pathway is considered a "biosynthetic hub" from which anabolism is fed. If a metabolite efflux is indeed occurring, anaplerotic reactions must keep a steady supply of substrates. In spite of this obvious relevance of anaplerosis, it has been poorly characterized in the malignant cell context. Glutaminolysis and and pyruvate carboxylation are two pathways that function in an anaplerotic fashion. In spite of the increasing evidence implicating these two processes in cancer metabolism their role as intermediate providers is overlooked. In this review we analyze the implications of an active anaplerosis in cancer and we discuss experimental evidence showing the relevance of these metabolic routes in tumor physiology.

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Section: The Existence Of Functional Mitochondria In Cancer?mentioning

confidence: 71%

Anaplerosis in cancer: Another step beyond the warburg effect

Ochoa-Ruiz¹,

Díaz-Ruiz²

2012

AJMB

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“…Therefore, it is of critical importance to develop an anti-cancer drugs with a defined target and integrated molecular mechanisms participated by distinct cancers [24]. Though not all tumor cells use glycolysis as their main energy source and mitochondrial metabolism is completely functional in these cells [137,138], they do exhibit a higher sensitivity to OXPHOS-inhibiting drugs than their normal counterparts [139]. Therefore, metabolic alterations appear to be a unique signature of diverse molecular abnormalities in tumors especially those with suppressed mitochondrial function [24].…”

Section: Blockage Of Glycolysismentioning

confidence: 99%

“…Metabolic therapy may have two advantages, namely 'specificity' and 'generality'. Specificity is referred to the reason why tumor cells are more sensitive to metabolic inhibitors than their normal coun-terparts [138,139]. Generality stands for its complete independence of specific signaling and/or epigenetic dysfunction [140].…”

Section: Blockage Of Glycolysismentioning

confidence: 99%

“…Generality stands for its complete independence of specific signaling and/or epigenetic dysfunction [140]. Glycolytic suppressors have been demonstrated to be successful in experimental tumor models exhibiting that the inhibition of glycolysis and/or OX-PHOS results in the delayed tumor growth and/or the impaired tumor cell viability in xenograft in nude mice and cell cultures in vitro [139,141]. As shown in the glycolysis pathway of the Figure 1, HK, PFK and PK are rate-limiting enzymes that catalyze three irreversible reactions in glycolytic pathway.…”

Section: Blockage Of Glycolysismentioning

confidence: 99%

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Glucose Metabolism in Breast Cancer and its Implication in Cancer Therapy

Li¹,

Tan²,

Li³

et al. 2011

IJCM

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“…Continued. - have pointed out the importance of the OXPHOS pathway in carcinogenesis and resistance to cancer therapy (28,29), and it has been suggested that loss of cell dependence on oxidative metabolism is an important factor in tumor development. In this line, it has been reported that drug-resistant tumors exhibit low oxidative phosphorylation and high glycolysis (30).…”

Section: ------------------------------------------------------------mentioning

confidence: 99%

Transcriptional changes induced by epigenetic therapy with hydralazine and magnesium valproate in cervical carcinoma

et al. 2011

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Abstract. Aberrant DNA methylation and histone deacetylation participate in cancer development and progression; hence, their reversal by inhibitors of DNA methylation and histone deacetylases is a promising cancer therapy. Experimental data demonstrate that these inhibitors in combination do not only show synergy in antitumor effects but also in whole genome global expression. Ten pairs of pre-and posttreatment cervical tumor samples were analyzed by microarray analysis. Treatment for seven days with hydralazine and valproate (HV) in patients up-regulated 964 genes. The two pathways possessing the highest number of up-regulated genes comprised the ribosome protein and the oxidative phosphorylation pathways, followed by MAPK signaling, tight junction, adherens junction, actin cytoskeleton, cell cycle, focal adhesion, apoptosis, proteasome, Wnt signaling, and antigen processing and presentation pathways. Upregulated genes by HV, clustered with down-regulated genes in untreated primary cervical carcinomas and were more alike as compared with up-regulated genes from untreated patients in terms of gene ontology. Increased acetylated p53 was also observed. Epigenetic therapy with HV leads to gene reactivation in primary tumors of cervical cancer patients as well as protein acetylation. A number of these reactivated genes have a definitive role as a tumor suppressors. The global expression pattern induced by HV suggests this therapy has an impact on pathways related to energy production which may promote apoptosis.

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Control of cellular proliferation by modulation of oxidative phosphorylation in human and rodent fast-growing tumor cells

Cited by 101 publications

References 52 publications

Anaplerosis in cancer: Another step beyond the warburg effect

Anaplerosis in cancer: Another step beyond the warburg effect

Glucose Metabolism in Breast Cancer and its Implication in Cancer Therapy

Transcriptional changes induced by epigenetic therapy with hydralazine and magnesium valproate in cervical carcinoma

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