ArticleInternational journal of medical sciences2012
Cytotoxicity of 15-deoxy-Δ(12,14)-prostaglandin J(2) through PPARγ-independent pathway and the involvement of the JNK and Akt pathway in renal cell carcinoma.
Article in International journal of medical sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Prolonged exposure to axitinib alters the molecular profile of Caki-2 renal cell carcinoma cells.Molecular and clinical oncology · 2025Article
- Dual function of activated PPARγ by ligands on tumor growth and immunotherapy.Medical oncology (Northwood, London, England) · 2024Review
- Renal Cell Cancer and Obesity.International journal of molecular sciences · 2022Review
- 15-deoxy-ΔBiochemistry and biophysics reports · 2019Article
- 15d-PGJ2 is a new hope for controlling tumor growth.American journal of translational research · 2018Review
- Peroxisome proliferator-activated receptors (PPARs) are potential drug targets for cancer therapy.Oncotarget · 2017Review
- Synergistic effects of 15-deoxy ΔBiochemistry and biophysics reports · 2017Article
- Article
- Metabolic syndrome and renal cell carcinoma.World journal of surgical oncology · 2014Review
- Cytotoxic effects of 15d-PGJ2 against osteosarcoma through ROS-mediated AKT and cell cycle inhibition.Oncotarget · 2014Article
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8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionAgonists of peroxisome proliferator-activated receptor gamma (PPARγ) have been examined as chemopreventive and chemotherapeutic agents. The aim was to investigate the cytotoxicity and action mechanisms of 15-deoxy-Δ(12,14)-prostaglandin J(2) (15d-PGJ(2)), one of endogenous ligands for PPARγ, in terms of PPARγ-dependency and the mitogen-activated protein kinase (MAPK) and Akt pathway in three human renal cell carcinoma (RCC)-derived cell lines.
methods786-O, Caki-2 and ACHN cells were used as human RCC-derived cell lines. Cell viability and caspase-3 activity was detected by fluorescent reagents, and chromatin-condensation was observed with a brightfield fluorescent microscope after staining cells with Hoechst33342. The expression levels of proteins were detected by Western blot analysis.
results15d-PGJ(2) showed cytotoxicity in dose-dependent manner. 15d-PGJ(2) induced chromatin-condensation and elevated caspase-3 activity, and the cell viability was restored by co-treatment with a pan-caspase inhibitor, Z-VAD-FMK, indicating the involvement of caspase-dependent apoptosis. The cytotoxicity was not impaired by a PPARγ inhibitor, GW9662, suggesting that 15d-PGJ(2) exerted the cytotoxicity in a PPARγ-independent manner. Some antioxidants rescued cells from cell death induced by 15d-PGJ(2), but some did not, suggesting that reactive oxygen species (ROS) did not contribute to the apoptosis. 15d-PGJ(2) also increased the expression levels of phospho-c-Jun N terminal kinase (JNK) in Caki-2 cells, and decreased those of phospho-Akt in 786-O cells, indicating that the JNK MAPK and the Akt pathways participated in the anticancer effects of 15d-PGJ(2) in some cell lines.
conclusion15d-PGJ(2) exerted cytotoxic effects accompanying caspase-dependent apoptosis, and this effect was elicited in a PPARγ-independent manner in three cell lines. In addition, the JNK MAPK and Akt pathway was involved in the cytotoxicity of 15d-PGJ(2) to some extent in some cell line. Therefore, our study showed the 15d-PGJ(2) to potentially be an interesting approach for RCC treatment.
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