Journal of Korean Endocrine Society 2004;19(5):511-521.
Published online October 1, 2004.
Role of Pexoxisome Proliferator Activated Receptor Gamma in Growth Regulation of Thyroid Cancer Cells.
Tae Yong Kim, Ja Young Song, Young Kee Shong, Won Bae Kim
1Department of Internal Medicine, Asan Medical Cencer, University of Ulsan College of Medicine, Korea.
2Asan Institute for Life Sciences, Seoul, Korea.
There is currently no effective option for the treatment of poorly differentiated thyroid carcinomas, so further studies are needed to evaluate new therapeutics. Thiazolinedione, an agonist of peroxisome proliferator activated receptor gamma (PPAR ), is known to suppress the growth of various tumor cell lines. This study was conducted to see if PPAR is involved in growth regulation of poorly differentiated thyroid cancer cells. SUBJECT AND METHODS: Thyroid cancer cell lines with a low degree differentiation, such as ARO and FRO cells were used, and their expression of PPAR mRNA checked. The effects of known agonists (rosiglitazone and 15-deoxy-delta12,14-prostglandin (15d-PGJ2)) and antagonists for PPAR (bisphenol A diglycidyl ether (BADGE)) on the growth of thyroid cancer cell lines expressing PPAR were evaluated by various methods, such as the methylthiazoletetrazolium bromide (MTT) assay, cell counts, and [3H]thymidine uptake. RESULTS: The expressions of PPAR were higher in ARO and FRO cells than in those of normal thyroid. Form the results of the MTT assay, the survival of ARO and FRO cells were found to decrease after administration of rosiglitazone or 15d-PGJ2. However, no change was observed after administration of BADGE. When the effect of rosiglitazone was evaluated by cell counting, there was significant decrease in number of ARO and FRO cells, but no change was observed after administration of 15d-PGJ2. Similar results were obtained using [3H]thymidine uptake. Thus, rosiglitazone treatment significantly decreased the [3H]thymidine uptake, whereas 15d-PGJ2 showed no significant effect. CONCLUSION: PPAR agonists (rosiglitazone and 15dPG-J2) suppressed the survival of ARO and FRO cells, undifferentiated thyroid cancer cell lines, with increased expressions of PPAR . However, the cell count and [3H] thymidine uptake were affected by rosiglitazone, but not by 15dPG-J2. This might suggest the antiproliferative effects of rosiglitazone are independent of PPAR ; and therefore, mediated by another unknown mechanism
Key Words: Prostaglandins, Thiazolidinediones, Thyroid Gland, Thyroid Neoplasms, Transcription Factors, Tumor Suppressor

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