ReviewFrontiers in oncology2018
Deciphering the Dichotomous Effects of PGC-1α on Tumorigenesis and Metastasis.
Review in Frontiers in oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
21 citing papers in PubMed, 43 citations in OpenAlex.
- Magnetic Reprogramming of Macrophages Stimulates Phagocytosis of Breast Cancer Cells via a TRPC1-STING Inflammatory Axis.Smart medicine · 2026Article
- Oxidative phosphorylation and breast cancer progression: insights into PGC-1α's role in mitochondrial function.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Anoikis resistance in Cancer: Mechanisms, therapeutic strategies, potential targets, and models for enhanced understanding.Cancer letters · 2025Review
- Knockdown of PGC1α suppresses dysplastic oral keratinocytes proliferation through reprogramming energy metabolism.International journal of oral science · 2023Article
- Association between PPARγ, PPARGC1A, and PPARGC1B genetic variants and susceptibility of gastric cancer in an Eastern Chinese population.BMC medical genomics · 2022Article
- Inducing respiratory complex I impairment elicits an increase in PGC1α in ovarian cancer.Scientific reports · 2022Article
- Whole-Genome Sequencing IdentifiesCancers · 2022Article
- PGC1α/β Expression Predicts Therapeutic Response to Oxidative Phosphorylation Inhibition in Ovarian Cancer.Cancer research · 2022Article
- Review
- Metabolism heterogeneity in melanoma fuels deactivation of immunotherapy: Predict before protect.Frontiers in oncology · 2022Review
- AdipoRon and Other Adiponectin Receptor Agonists as Potential Candidates in Cancer Treatments.International journal of molecular sciences · 2021Review
- The emerging role of estrogen related receptorα in complications of non-small cell lung cancers.Oncology letters · 2021Review
- Biomolecular Condensates and Cancer.Cancer cell · 2021Review
- Combined Targeting of Estrogen Receptor Alpha and Exportin 1 in Metastatic Breast Cancers.Cancers · 2020Article
- Oxidative Stress in Cancer.Cancer cell · 2020Review
- Editorial: Epithelial-Mesenchymal Transition: Yet Another Exciting Avenue in Cancer Metabolic Remodeling.Frontiers in oncology · 2020Article
- Metabolic adaptations in spontaneously immortalized PGC-1α knock-out mouse embryonic fibroblasts increase their oncogenic potential.Redox biology · 2020Article
- Metabolic adaptability in metastatic breast cancer by AKR1B10-dependent balancing of glycolysis and fatty acid oxidation.Nature communications · 2019Article
- Review
- The PGC-1/ERR network and its role in precision oncology.NPJ precision oncology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic reprogramming confers cancer cells the ability to grow and survive under nutrient-depleted or stressful microenvironments. The amplification of oncogenes, the loss of tumor suppressors, as well as context- and lineage-specific determinants can converge and profoundly affect the metabolic status of cancer cells. Cumulating evidences suggest that highly glycolytic cells under the influence of oncogenes such as BRAF, or evolving in hypoxic microenvironments, will promote metastasis through modulation of multiple steps of tumorigenesis such as the epithelial-to-mesenchymal transition (EMT). On the contrary, increased reliance on mitochondrial respiration is associated with hyperplasic rather than metastatic disease. The PGC-1α transcriptional coactivator, a master regulator of mitochondrial biogenesis, has recently been shown to exert antimetastatic effects in cancer, notably through inhibition of EMT. Besides, PGC-1α has the opposite role in specific cancer subtypes, in which it appears to provide growth advantages. Thus, the regulation and role of PGC-1α in cancer is not univocal, and its use as a prognostic marker appears limited given its highly dynamic nature and its multifaceted regulation by transcriptional and posttranslational mechanisms. Herein, we expose key oncogenic and lineage-specific modules that finely regulate PGC-1α to promote or dampen the metastatic process. We propose a unifying model based on the systematic analysis of its controversial implication in cancer from cell proliferation to EMT and metastasis. This short review will provide a good understanding of current challenges associated with the study of PGC-1α.
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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.