Troglitazone Increases the Susceptibility to TRAIL-Induced Apoptosis in Thyroid Cancer Cell Lines.
10.16956/kjes.2003.3.2.113
- Author:
Jin Woo PARK
1
;
Orlo H CLARK
Author Information
1. Department of Surgery, Chungbuk National University, Cheongju, Korea.
- Publication Type:Original Article
- Keywords:
TRAIL;
Apoptosis;
PPARγ;
Thyroid cancer
- MeSH:
Apoptosis*;
Cell Death;
Cell Line*;
Flow Cytometry;
Humans;
Thyroid Gland*;
Thyroid Neoplasms*;
Tumor Necrosis Factor-alpha
- From:Korean Journal of Endocrine Surgery
2003;3(2):113-120
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Tumor necrosis factor related apoptosis-inducing ligand (TRAIL) induces apoptosis in many human cancer cells but not in normal cells. Thyroid cancer cells, however, appear to be relatively resistant to TRAIL-induced apoptosis. We investigated the effect of troglitazone, a PPARγ agonist, on TRAIL-induced apoptosis in thyroid cancer cells. METHODS: We used 6 thyroid cancer cell lines: TPC-1, FTC- 133, FTC-236, FTC-238, XTC-1, and ARO82-1. We used flow cytometry to detect apoptosis and used MTT assay to measure anti-proliferation effects. ANOVA was used for statistical analysis. RESULTS: TPC-1 cells were the most sensitive to soluble TRAIL. FTC-133 and ARO82-1 were resistant to TRAIL and growth inhibition was less than 20% at concentration of 800 ng/ml of TRAIL. In both TPC-1 (TRAIL-sensitive) and FTC- 133 (TRAIL-resistant) thyroid cancer cell lines, pretreatment with troglitazone enhanced TRAIL-induced cell death significantly. Bcl-family proteins did not seem to be involved in sensitization of TRAIL-induced apoptosis by troglitazone. CONCLUSION: TRAIL in combination with troglitazone induces apoptosis in thyroid cancer cells at suboptimal concentrations that can not be achieved using TRAIL alone.
