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Open AccessJournal ArticleDOI

Increases in mitochondrial biogenesis impair carcinogenesis at multiple levels

Xiao Wang, +1 more
- 01 Oct 2011 - 
- Vol. 5, Iss: 5, pp 399-409
TLDR
By increasing the efficiency of the mitochondrial oxidative phosphorylation system, cancer progression is hampered by decreases in cell proliferation and invasiveness.
About
This article is published in Molecular Oncology.The article was published on 2011-10-01 and is currently open access. It has received 65 citations till now. The article focuses on the topics: Mitochondrial biogenesis & Mitochondrion.

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Oncogenic BRAF Regulates Oxidative Metabolism via PGC1α and MITF

TL;DR: It is shown that BRAF inhibition also induces an oxidative phosphorylation gene program, mitochondrial biogenesis, and the increased expression of the mitochondrial master regulator, PGC1α, and a target of BRAF, the melanocyte lineage factor MITF, directly regulates the expression of P GC1α.

Evidence for an Alternative Glycolytic Pathway in Rapidly Proliferating Cells

TL;DR: In this paper, the authors demonstrate that phosphoenolpyruvate (PEP) can act as a phosphate donor in mammalian cells because PEP participates in the phosphorylation of the glycolytic enzyme phosphoglycerate mutase (PGAM1) in PKM2-expressing cells.
Journal ArticleDOI

After the banquet: Mitochondrial biogenesis, mitophagy, and cell survival

TL;DR: It is concluded that in primary neurons and other mitochondrially dependent cells, disruptions in any phase of the mitochondrial recycling process can contribute to cellular dysfunction and disease.
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PGC-1α as a Pivotal Factor in Lipid and Metabolic Regulation.

TL;DR: It is demonstrated that PGC-1α plays a central role in coordinating the gene expression of key components of mitochondrial biogenesis and as a critical metabolic regulator in many vital organs, including white and brown adipose tissue, skeletal muscle, heart, liver, and kidney.
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MitoTALEN: A General Approach to Reduce Mutant mtDNA Loads and Restore Oxidative Phosphorylation Function in Mitochondrial Diseases

TL;DR: Short versions of the mitoTALEN specific for the MERRF m.8344A>G mutation are designed, which will improve the ability to package these large sequences into viral vectors, bringing the use of these genetic tools closer to clinical trials.
References
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Journal ArticleDOI

Why do cancers have high aerobic glycolysis

TL;DR: In this article, the authors propose that persistent metabolism of glucose to lactate even in aerobic conditions is an adaptation to intermittent hypoxia in pre-malignant lesions, which leads to microenvironmental acidosis requiring evolution to phenotypes resistant to acid-induced cell toxicity.
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The metabolism of tumors in the body.

TL;DR: The question of whether tumor cells in living animals can be killed off through lack of energy, and the related question of how the tumors are supplied with oxygen and glucose in the body are discussed.
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Sulforhodamine B colorimetric assay for cytotoxicity screening

TL;DR: The sulforhodamine B (SRB) assay is used for cell density determination, based on the measurement of cellular protein content, which is an efficient and highly cost-effective method for screening.
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Suppression of Reactive Oxygen Species and Neurodegeneration by the PGC-1 Transcriptional Coactivators

TL;DR: Increase in PGC-1alpha levels dramatically protects neural cells in culture from oxidative-stressor-mediated death, providing a potential target for the therapeutic manipulation of these important endogenous toxins.
Journal ArticleDOI

Succinate links TCA cycle dysfunction to oncogenesis by inhibiting HIF-α prolyl hydroxylase

TL;DR: A mitochondrion-to-cytosol signaling pathway that links mitochondrial dysfunction to oncogenic events is described, suggesting a mechanistic link between SDH mutations and HIF-1alpha induction, providing an explanation for the highly vascular tumors that develop in the absence of VHL mutations.
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