ArticlePPAR research2008
Mitochondria, PPARs, and Cancer: Is Receptor-Independent Action of PPAR Agonists a Key?
Article in PPAR research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 44 citations in OpenAlex.
- Induction of Cyp450 enzymes by 4-thiazolidinone-based derivatives in 3T3-L1 cells in vitro.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
- Medicinal Chemistry Targeting Mitochondria: From New Vehicles and Pharmacophore Groups to Old Drugs with Mitochondrial Activity.International journal of molecular sciences · 2020Review
- The Effect of Biotinylated PAMAM G3 Dendrimers Conjugated with COX-2 Inhibitor (celecoxib) and PPARγ Agonist (Fmoc-L-Leucine) on Human Normal Fibroblasts, Immortalized Keratinocytes and Glioma Cells in Vitro.Molecules (Basel, Switzerland) · 2019Article
- Chemically Modified Variants of Fenofibrate with Antiglioblastoma Potential.Translational oncology · 2019Article
- Telmisartan induces melanoma cell apoptosis and synergizes with vemurafenibCancer biology & medicine · 2019Article
- Fenofibrate Augments the Sensitivity of Drug-Resistant Prostate Cancer Cells to Docetaxel.Cancers · 2019Article
- Article
- Pivotal Roles of Peroxisome Proliferator-Activated Receptors (PPARs) and Their Signal Cascade for Cellular and Whole-Body Energy Homeostasis.International journal of molecular sciences · 2018Review
- Dysbiosis of gut microbiota in promoting the development of colorectal cancer.Gastroenterology report · 2018Review
- NF-κB/RelA-PKM2 mediates inhibition of glycolysis by fenofibrate in glioblastoma cells.Oncotarget · 2015Article
- Peroxisome proliferator activated receptor α ligands as anticancer drugs targeting mitochondrial metabolism.Current pharmaceutical biotechnology · 2013Review
- PPARs: Interference with Warburg' Effect and Clinical Anticancer Trials.PPAR research · 2012Article
- PPARG Epigenetic Deregulation and Its Role in Colorectal Tumorigenesis.PPAR research · 2012Article
- Article
- Bimodal targeting of microsomal cytochrome P450s to mitochondria: implications in drug metabolism and toxicity.Expert opinion on drug metabolism & toxicology · 2010Review
- Synergism in hyperhomocysteinemia and diabetes: role of PPAR gamma and tempol.Cardiovascular diabetology · 2010Article
- ROS accumulation and IGF-IR inhibition contribute to fenofibrate/PPARalpha -mediated inhibition of glioma cell motility in vitro.Molecular cancer · 2010Article
- Long chain acyl-CoA synthetase-3 is a molecular target for peroxisome proliferator-activated receptor delta in HepG2 hepatoma cells.The Journal of biological chemistry · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Before the discovery of peroxisome proliferator activated receptors (PPARs), it was well known that certain drugs considered as classical PPAR-alpha agonists induced hepatocarcinoma or peroxisome proliferation in rodents. These drugs were derivatives of fibric acid, and they included clofibrate, bezafibrate, and fenofibrate. However, such toxicity has never been observed in human patients treated with these hypolipidemic drugs. Thiazolidinediones are a new class of PPAR activators showing greater specificity for the gamma isoform of PPARs. These drugs are used as insulin sensitizers in the treatment of type II diabetes. In addition, they have been shown to induce cell differentiation or apoptosis in various experimental models of cancer. PPAR-alpha ligands have also been shown to induce cancer cell differentiation and, paradoxically, PPAR-gamma drug activators have been reported to act as carcinogens. The confusing picture that emerges from these data is further complicated by the series of intriguing side effects observed following administration of pharmacological PPAR ligands (rhabdomyolysis, liver and heart toxicity, anemia, leucopenia). These side effects cannot be easily explained by simple interactions between the drug and nuclear receptors. Rather, these side effects seem to indicate that the ligands have biological activity independent of the nuclear receptors. Considering the emerging role of mitochondria in cancer and the potential metabolic connections between this organelle and PPAR physiology, characterization of the reciprocal influences is fundamental not only for a better understanding of cancer biology, but also for more defined pharmacotoxicological profiles of drugs that modulate PPARs.
Identifiers
What OpenQuestion holds
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.