ArticleCancer biology & therapy2011
Troglitazone suppresses c-Myc levels in human prostate cancer cells via a PPARγ-independent mechanism.
Article in Cancer biology & therapy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 55 citations in OpenAlex.
- Targeting Prostate Cancer Metabolism Through Transcriptional and Epigenetic Modulation: A Multi-Target Approach to Therapeutic Innovation.International journal of molecular sciences · 2025Review
- The KDM5 inhibitor PBIT reduces proliferation of castration-resistant prostate cancer cells via cell cycle arrest and the induction of senescence.Experimental cell research · 2024Article
- The role of PPARγ in prostate cancer development and progression.British journal of cancer · 2023Review
- Pioglitazone and Prostate Cancer Risk in Taiwanese Male Patients with Type 2 Diabetes: A Retrospective Cohort Study.The world journal of men's health · 2023Article
- Canagliflozin alleviates valproic acid-induced autism in rat pups: Role of PTEN/PDK/PPAR-γ signaling pathways.Frontiers in pharmacology · 2023Article
- Review
- Peroxisome Proliferator-Activated Receptors as Molecular Links between Caloric Restriction and Circadian Rhythm.Nutrients · 2020Review
- Review
- PPARγ agonists: potential treatment for autism spectrum disorder by inhibiting the canonical WNT/β-catenin pathway.Molecular psychiatry · 2019Review
- Enteric Microbiota⁻Gut⁻Brain Axis from the Perspective of Nuclear Receptors.International journal of molecular sciences · 2018Review
- A Sterol from Soft Coral Induces Apoptosis and Autophagy in MCF-7 Breast Cancer Cells.Marine drugs · 2018Article
- Pro-apoptotic effects of Kangfuxin on human stomach cancer cells and its underlying mechanism.Oncology letters · 2018Article
- Interplay between the renin-angiotensin system, the canonical WNT/β-catenin pathway and PPARγ in hypertension.Current hypertension reports · 2018Review
- Demyelination in Multiple Sclerosis: Reprogramming Energy Metabolism and Potential PPARγ Agonist Treatment Approaches.International journal of molecular sciences · 2018Review
- Crosstalk Between Peroxisome Proliferator-Activated Receptor Gamma and the Canonical WNT/β-Catenin Pathway in Chronic Inflammation and Oxidative Stress During Carcinogenesis.Frontiers in immunology · 2018Review
- Interactions between TGF-β1, canonical WNT/β-catenin pathway and PPAR γ in radiation-induced fibrosis.Oncotarget · 2017Review
- Macrocyclic peptides decrease c-Myc protein levels and reduce prostate cancer cell growth.Cancer biology & therapy · 2017Article
- Crosstalk between the Androgen Receptor and PPAR Gamma Signaling Pathways in the Prostate.PPAR research · 2017Review
- Modulation of glycogen synthase kinase-3β following TRAIL combinatorial treatment in cancer cells.Oncotarget · 2016Article
- Tumor Necrosis Factor-related Apoptosis-inducing Ligand (TRAIL)-Troglitazone-induced Apoptosis in Prostate Cancer Cells Involve AMP-activated Protein Kinase.The Journal of biological chemistry · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Troglitazone is a ligand for the peroxisome proliferator activated receptor gamma (PPARγ) that decreases growth of human prostate cancer cells in vitro and in vivo. However, the mechanism by which troglitazone reduces prostate cancer cell growth is not fully understood. To understand the signaling pathways involved in troglitazone-induced decreases in prostate cancer growth, we examined the effect of troglitazone on androgen-independent C4-2 human prostate cancer cells. Initial experiments revealed troglitazone inhibited C4-2 cell proliferation by arresting cells in the G(0)/G(1) phase of the cell cycle and inducing apoptosis. Since the proto-oncogene product c-Myc regulates both apoptosis and cell cycle progression, we next examined whether troglitazone altered expression of c-Myc. Troglitazone decreased c-Myc protein levels as well as expression of downstream targets of c-Myc in a dose-dependent manner. In C4-2 cells, troglitazone-induced decreases in c-Myc protein involve proteasome-mediated degradation of c-Myc protein as well as reductions in c-Myc mRNA levels. It appears that troglitazone stimulates degradation of c-Myc by increasing c-Myc phosphorylation, for the level of phosphorylated c-Myc was elevated in prostate cancer cells exposed to troglitazone. While troglitazone dramatically decreased the amount of c-Myc within C4-2 cells, the PPARγ ligands ciglitazone, rosiglitazone and pioglitazone did not reduce c-Myc protein levels. Furthermore the down-regulation of c-Myc by troglitazone was not blocked by the PPARγ antagonist GW9662 and siRNA-mediated decreases in PPARγ protein. Thus, our data suggest that troglitazone reduces c-Myc protein independently of PPARγ.
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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.