ArticleOncotarget2016
Activation of PPARγ suppresses proliferation and induces apoptosis of esophageal cancer cells by inhibiting TLR4-dependent MAPK pathway.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 53 citations in OpenAlex.
- Parallel adaptation to geothermally-warmed habitats due to common structural variation and functional developmental pathways.Nature communications · 2026Article
- Review
- Bioinformatic analysis and experimental validation of the function of mitogen-activated protein kinase in esophageal cancer.Discover oncology · 2026Article
- Dual Modulation of Adipogenesis and Apoptosis by PPARG Agonist Rosiglitazone and Antagonist Betulinic Acid in 3T3-L1 Cells.Biomedicines · 2025Article
- Reassessing the Role of Tissue Factor Pathway Inhibitor 2 in Neoplastic and Non-Neoplastic Lesions.Cancers · 2025Review
- PPAR-γ in Melanoma and Immune Cells: Insights into Disease Pathogenesis and Therapeutic Implications.Cells · 2025Review
- TLR4 Targeting: A Promising Therapeutic Approach Across Multiple Human Diseases.Current protein & peptide science · 2025Review
- Toll-like Receptor 4 Signaling Mediates Gastritis and Gastric Cancer.Current molecular medicine · 2025Review
- A nonsteroidal anti-inflammatory drug, zaltoprofen, inhibits the growth of extraskeletal chondrosarcoma cells by inducing PPARγ, p21, p27, and p53.Cell cycle (Georgetown, Tex.) · 2023Article
- Demethoxycurcumin represses cervical cancer growth through PPARγ-regulated proliferation and apoptosis.Acta biochimica et biophysica Sinica · 2023Article
- Peroxisome proliferator-activated receptors regulate the progression and treatment of gastrointestinal cancers.Frontiers in pharmacology · 2023Review
- The Role of PPARs in Breast Cancer.Cells · 2022Review
- Bioinformatics analysis reveals the potential target of rosiglitazone as an antiangiogenic agent for breast cancer therapy.BMC genomic data · 2022Article
- Oral Microbiota Variation: A Risk Factor for Development and Poor Prognosis of Esophageal Cancer.Digestive diseases and sciences · 2022Review
- TLR4 and SARM1 modulate survival and chemoresistance in an HPV-positive cervical cancer cell line.Scientific reports · 2022Article
- A Metabolomics Investigation of the Metabolic Changes of Raji B Lymphoma Cells Undergoing Apoptosis Induced by Zinc Ions.Metabolites · 2021Article
- Adipocyte-Specific ACKR3 Regulates Lipid Levels in Adipose Tissue.Biomedicines · 2021Article
- PPAR-γ Modulators as Current and Potential Cancer Treatments.Frontiers in oncology · 2021Review
- Important players in carcinogenesis as potential targets in cancer therapy: an update.Oncotarget · 2020Review
- Activation of PPARγ Inhibits TLR4 Signal Transduction Pathway in Melanoma CancerAdvanced pharmaceutical bulletin · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although substantial studies on peroxisome proliferator-activated receptor g (PPARg) have focused on the mechanisms by which PPARg regulates glucose and lipid metabolism, recent reports have suggested that PPARg shows tumorigenic or antitumorigenic effects. The roles and mechanisms of PPARg activation in esophageal cancer remain unclarified. EC109 and TE10 esophageal cancer cells were treated with 0, 10, 20 and 40 mM of PPARg agonist rosiglitazone (RGZ) for 24, 48, and 72 h, and the cell viability and apoptosis were detected using methyl thiazolyl tetrazolium (MTT) assay and Flow cytometric (FCM) analysis, respectively. Moreover, the effects of inhibition of PPARg by antagonist or specific RNA interference on cell viability, apoptosis, the Toll-like receptor 4 (TLR4) and mitogen-activated protein kinase (MAPK) pathways were evaluated. Additionally, the effect of TLR4 signaling on the MAPK pathway, cell viability and apoptosis was assessed. The results showed that RGZ suppressed proliferation and induced apoptosis of esophageal cancer cells, which could be partly restored by inactivation of PPARg. RGZ suppressed the MAPK and TLR4 pathways, and the inhibitory effect could be counteracted by PPARg antagonist or specific RNA interference. We also suggested that MAPK activation was regulated by the TLR4 pathway and that blocking the TLR4 and MAPK pathways significantly suppressed proliferation and induced apoptosis of esophageal cancer cells. In conclusion, our data suggested that activation of PPARg suppressed proliferation and induced apoptosis of esophageal cancer cells by inhibiting TLR4-dependent MAPK pathway.
Indexed as
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.