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Modulation of cell growth and PPARgamma expression in human colorectal cancer cell lines by ciglitazone
Nik Soriani Yaacob1, Halisa Mohd Darus, Mohd Nor Norazmi
1Department of Chemical Pathology, School of Medical Sciences, Universiti Sains Malaysia, 16150 Kubang Kerian, Kelantan, Malaysia. soriani@kb.usm.my
Abstract:
Studies have shown that ligand activation of peroxisome proliferator-activated receptor gamma (PPARgamma) can induce differentiation and inhibit proliferation of several cancer cells. The present study was performed to investigate the effects of the PPARgamma ligand, ciglitazone, and the involvement of PPARgamma in modulating the growth of human colorectal cancer cells. Lactate dehydrogenase release assay showed that ciglitazone potently inhibited HT-29 (well-differentiated) and COLO-205 (poorly differentiated) colorectal adenocarcinoma cell growth. Measurement of apoptosis by flow cytometry using a fluorescein-conjugated monoclonal antibody against cytokeratin 18 revealed a high induction of apoptosis by ciglitazone in a time-dependent fashion. The expression of PPARgamma1 but not PPARgamma2 mRNA was significantly downregulated as measured by real-time quantitative PCR, and the PPARgamma protein levels were decreased as determined by Western blot analysis. We conclude that ciglitazone treatment suppressed colon cancer cell growth via induction of apoptosis. However, the anticancer effects of ciglitazone may not depend solely on PPARgamma activation.
Insights
Ciglitazone, a PPARgamma ligand, suppressed colon cancer cell growth and induced apoptosis. However, its anticancer effects may involve pathways beyond PPARgamma activation.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Peroxisome proliferator-activated receptor gamma (PPARgamma) ligand activation can inhibit cancer cell proliferation and induce differentiation.
- PPARgamma plays a role in modulating human colorectal cancer cell growth.
Purpose of the Study:
- To investigate the effects of the PPARgamma ligand, ciglitazone, on human colorectal cancer cell growth.
- To determine the involvement of PPARgamma in mediating ciglitazone's effects on colon cancer cells.
Main Methods:
- Lactate dehydrogenase release assay to assess cell viability.
- Flow cytometry with anti-cytokeratin 18 antibody to measure apoptosis.
- Real-time quantitative PCR and Western blot analysis to evaluate PPARgamma expression.
Main Results:
- Ciglitazone potently inhibited the growth of both well-differentiated (HT-29) and poorly differentiated (COLO-205) colorectal cancer cells.
- Ciglitazone induced apoptosis in a time-dependent manner.
- PPARgamma1 mRNA expression was downregulated, and PPARgamma protein levels decreased following ciglitazone treatment.
Conclusions:
- Ciglitazone treatment suppresses colon cancer cell growth through apoptosis induction.
- The anticancer effects of ciglitazone may not be solely dependent on PPARgamma activation.
