ArticleLipids in health and disease2022
WY-14643 attenuates lipid deposition via activation of the PPARα/CPT1A axis by targeting Gly335 to inhibit cell proliferation and migration in ccRCC.
Article in Lipids in health and disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 20 citations in OpenAlex.
- Research progress in metabolic reprogramming and targeting metabolic pathways for clear cell renal cell carcinoma.Genes & diseases · 2026Review
- Cannabigerol and Cannabichromene Induce Lung Cancer Cell Death and Apoptosis-Contribution of PPARα to Cannabigerol Effects.Antioxidants (Basel, Switzerland) · 2026Article
- PPARα activation alleviates lithocholic acid-induced liver injury by inhibiting pyroptosis.Liver research (Beijing, China) · 2026Article
- Integrating Network Pharmacology and Experimental Validation of Oleanolic Acid Targeting the PPARα-CPT1A Axis to Modulate Lipid Metabolism in Hepatocellular Carcinoma Cells.International journal of molecular sciences · 2026Article
- Deciphering the molecular networks of 3-methylcholanthrene-induced clear cell renal cell carcinoma through multi-omics integration.Scientific reports · 2026Article
- Daixie recipe ameliorates diet-induced MASH in miceFrontiers in endocrinology · 2026Article
- TFE3 fusion proteins driveFrontiers in immunology · 2026Article
- Lipid reprogramming and ferroptosis crosstalk in clear cell renal cell carcinoma: metabolic vulnerabilities and therapeutic targeting.Molecular cancer · 2025Review
- MicroRNA-372-3p impairs fatty acid metabolism in hepatocellular carcinoma cells by targetingBioImpacts : BI · 2025Article
- Hypoglycemic Agents Increase Regulatory Factor X1 to Inhibit Cancer Cell Behaviour in Human Glioblastoma Cells.Journal of cellular and molecular medicine · 2024Article
- Weighted gene co-expression network analysis identified GBP2 connected to PPARα activity and liver cancer.Scientific reports · 2024Article
- Discovering the lipid metabolism-related hub genes of HCC-treated samples with PPARα agonist through weighted correlation network analysis.Scientific reports · 2024Article
- Current View on PPAR-α and Its Relation to Neurosteroids in Alzheimer's Disease and Other Neuropsychiatric Disorders: Promising Targets in a Therapeutic Strategy.International journal of molecular sciences · 2024Review
- Deficiency of SDHC promotes metastasis by reprogramming fatty acid metabolism in colorectal cancer.Journal of translational medicine · 2024Article
- Novel Effect ofMolecules (Basel, Switzerland) · 2023Article
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8 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundHistologically, cytoplasmic deposits of lipids and glycogen are common in clear cell renal cell carcinoma (ccRCC). Owing to the significance of lipid deposition in ccRCC, numerous trials targeting lipid metabolism have shown certain therapeutic potential. The agonism of peroxisome proliferator-activated receptor-α (PPARα) via ligands, including WY-14,643, has been considered a promising intervention for cancers.
methodsFirst, the effects of WY-14,643 on malignant behaviors were investigated in ccRCC in vitro. After RNA sequencing, the changes in lipid metabolism, especially neutral lipids and glycerol, were further evaluated. Finally, the underlying mechanisms were revealed.
resultsPhenotypically, the proliferation and migration of ccRCC cells treated with WY-14,643 were significantly inhibited in vitro. A theoretical functional mechanism was proposed in ccRCC: WY-14,643 mediates lipid consumption by recognizing carnitine palmitoyltransferase 1 A (CPT1A). Activation of PPARα using WY-14,643 reduces lipid deposition by increasing the CPT1A level, which also suppresses the NF-κB signaling pathway. Spatially, WY-14,643 binds and activates PPARα by targeting Gly335.
conclusionOverall, WY-14,643 suppresses the biological behaviors of ccRCC in terms of cell proliferation, migration, and cell cycle arrest. Furthermore, its anticancer properties are mediated by the inhibition of lipid accumulation, at least in part, through the PPARα/CPT1A axis by targeting Gly335, as part of the process, NF-κB signaling is also suppressed. Pharmacological activation of PPARα might offer a new treatment option for ccRCC.
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