ArticleMolecular oncology2011
Increases in mitochondrial biogenesis impair carcinogenesis at multiple levels.
Article in Molecular oncology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 66 citations in OpenAlex.
- CRAT downregulation promotes ovarian cancer progression by facilitating mitochondrial metabolism through decreasing the acetylation of PGC-1α.Cell death discovery · 2025Article
- Mitochondria: a new intervention target for tumor invasion and metastasis.Molecular medicine (Cambridge, Mass.) · 2024Review
- Remdesivir increases mtDNA copy number causing mild alterations to oxidative phosphorylation.Scientific reports · 2023Article
- The Mitochondrial ATP Synthase/IF1 Axis in Cancer Progression: Targets for Therapeutic Intervention.Cancers · 2023Review
- PGC-1α Is a Master Regulator of Mitochondrial Lifecycle and ROS Stress Response.Antioxidants (Basel, Switzerland) · 2023Review
- Deregulated transcription factors in cancer cell metabolisms and reprogramming.Seminars in cancer biology · 2022Review
- The relationship between epigenetic age and the hallmarks of aging in human cells.Nature aging · 2022Article
- An amino acid-defined diet impairs tumour growth in mice by promoting endoplasmic reticulum stress and mTOR inhibition.Molecular metabolism · 2022Article
- Mito-FUNCAT-FACS reveals cellular heterogeneity in mitochondrial translation.RNA (New York, N.Y.) · 2022Article
- Review
- [High-mobility group protein 1 promotes diethylnitrosamine-induced liver cancer formation in mice by activating mitochondrial biogenesis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2020Article
- From old to new - Repurposing drugs to target mitochondrial energy metabolism in cancer.Seminars in cell & developmental biology · 2020Review
- Review
- Posttranslational regulation of PGC-1α and its implication in cancer metabolism.International journal of cancer · 2019Review
- Article
- PGC-1α as a Pivotal Factor in Lipid and Metabolic Regulation.International journal of molecular sciences · 2018Review
- Peroxisome Proliferator-Activated ReceptorPPAR research · 2018Review
- Agent-Based Modeling of Mitochondria Links Sub-Cellular Dynamics to Cellular Homeostasis and Heterogeneity.PloS one · 2017Article
- Article
- Mitochondrial DNA damage induced autophagy, cell death, and disease.Frontiers in bioscience (Landmark edition) · 2016Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Although mitochondrial respiration is decreased in most cancer cells, the role of this decrease in carcinogenesis and cancer progression is still unclear. To better understand this phenomenon, instead of further inhibiting mitochondrial function, we induced mitochondrial biogenesis in transformed cells by activating the peroxisome proliferator-activated receptors (PPARs)/peroxisome proliferator-activated receptor gamma co-activator 1α (PGC-1α) pathways. This was achieved by treating the cells with bezafibrate, a PPARs panagonist that also enhances PGC-1α expression. We confirmed that bezafibrate treatment led to increased mitochondrial proteins and enzyme functions. We found that cells with increased mitochondrial biogenesis had decreased growth rates in glucose-containing medium. In addition, they became less invasive, which was directly linked to the reduced lactate levels. Surprisingly, even though bezafibrate-treated cells had higher levels of mitochondrial markers, total respiration was not significantly altered. However, respiratory coupling, and ATP levels were. Our data show that by increasing the efficiency of the mitochondrial oxidative phosphorylation system, cancer progression is hampered by decreases in cell proliferation and invasiveness.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.