ArticleJournal of the National Cancer Institute2014
Potentiation of colon cancer susceptibility in mice by colonic epithelial PPAR-δ/β overexpression.
Article in Journal of the National Cancer Institute, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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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.
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Who cites it
35 citing papers in PubMed, 56 citations in OpenAlex.
- Compartment-specific PPARδ activity controls the outcome of cancer-immune cell competition and immunotherapy efficacy.Nature immunology · 2026Article
- PPARδ: An underappreciated tumor accelerator in pancreatic ductal adenocarcinoma.Cancer letters · 2026Review
- Article
- Regulatory role of PPAR in colorectal cancer.Cell death discovery · 2025Review
- Delineating the role of nuclear receptors in colorectal cancer, a focused review.Discover oncology · 2024Review
- Innovative strategies to optimise colorectal cancer immunotherapy through molecular mechanism insights.Frontiers in immunology · 2024Article
- PPARδ dysregulation of CCL20/CCR6 axis promotes gastric adenocarcinoma carcinogenesis by remodeling gastric tumor microenvironment.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2023Article
- PPAR-δ as a prognostic biomarker and its association with immune infiltrates in breast cancer PPAR-δ as a prognostic biomarker and its association with immune infiltrates in breast cancer.Journal of Cancer · 2023Article
- Review
- Identifying the Metabolic Signatures of PPARD-Overexpressing Gastric Tumors.International journal of molecular sciences · 2022Article
- Quercetin Inhibits KBM7R Cell Proliferation through Wnt/Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Targeting Adrenergic Receptors in Metabolic Therapies for Heart Failure.International journal of molecular sciences · 2021Review
- Influence of Lipoxygenase Inhibition on Glioblastoma Cell Biology.International journal of molecular sciences · 2020Article
- PPARδ is a regulator of autophagy by its phosphorylation.Oncogene · 2020Article
- PPAR Beta/Delta and the Hallmarks of Cancer.Cells · 2020Review
- ISG20 serves as a potential biomarker and drives tumor progression in clear cell renal cell carcinoma.Aging · 2020Article
- Kinase activity of ERBB3 contributes to intestinal organoids growth and intestinal tumorigenesis.Cancer science · 2020Article
- PPARδ Mediates the Effect of Dietary Fat in Promoting Colorectal Cancer Metastasis.Cancer research · 2019Article
- PPARD and Interferon Gamma Promote Transformation of Gastric Progenitor Cells and Tumorigenesis in Mice.Gastroenterology · 2019Article
- Pleiotropic Effects of PPARD Accelerate Colorectal Tumorigenesis, Progression, and Invasion.Cancer research · 2019Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe nuclear receptor peroxisome proliferator-activated receptor-δ/β (PPAR-d) is upregulated in human colorectal cancers, but its role in colonic tumorigenesis remains controversial.
methodsWe generated a novel mouse model of intestinally targeted PPAR-d overexpression to simulate PPAR-d upregulation in human colon carcinogenesis. Colon-specific PPAR-d overexpression was confirmed by real-time reverse transcription polymerase chain reaction, immunoblotting, and activity assays. Mice with and without targeted PPAR-d overexpression were tested for azoxymethane (AOM)-induced colonic tumorigenesis. Mouse whole-genome transcriptome microarray analyses were performed to identify PPAR-d target genes to promote tumorigenesis. We used linear models to test for PPAR-d overexpression trend effects on tumor multiplicity. All statistical tests were two-sided.
resultsTargeted PPAR-d overexpression markedly increased colonic tumor incidence (from 0 of 10 wild-type [WT] littermate mice to 9 of 10 mice [P < .001] in 2 FVB/N background mouse lines [villin-PPAR-d-1 and villin-PPAR-d-2] at a 5-mg/kg AOM dose) and multiplicity (number of tumors per mouse per mg/kg dose of AOM increased from 0.47 [95% confidence interval [CI] = 0.22 to 0.72] for the WT littermates to 2.15 [95% CI = 1.90 to 2.40] [P < .001] for the villin-PPAR-d-1 mice and from 0.44 [95% CI = 0.09 to 0.79] for the WT littermates to 1.91 [95% CI = 1.57 to 2.25] [P < .001] for the villin-PPAR-d-2 mice). PPAR-d overexpression reversed resistance to AOM-induced colonic tumorigenesis in C57BL/6 mice. PPAR-d overexpression modulated expression of several novel PPAR-d target genes in normal-appearing colonic epithelial cells of mice with PPAR-d overexpression in a pattern that matched the changes in colonic tumors.
conclusionsOur finding that PPAR-d upregulation profoundly enhances susceptibility to colonic tumorigenesis should impact the development of strategies of molecularly targeting PPAR-d in cancer and noncancerous diseases.
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