Endocrinol Metab > Volume 22(1); 2007 > Article
Journal of Korean Endocrine Society 2007;22(1):35-44.
DOI: https://doi.org/10.3803/jkes.2007.22.1.35    Published online February 1, 2007.
Effects of Wnt-1 on the Growth and Apoptosis of FRTL-5 Cells.
Jung Min Kim, Tae Yong Kim, Young Kee Shong, Yoon Soo Rhee, Eun Jung Park, Hyun Chung Choi, Won Bae Kim
1Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Korea.
2Asan Institute for Life Sciences, University of Ulsan College of Medicine, Korea.
Abstract
BACKGROUND
Wnt proteins are major signaling molecules involved in embryonic induction, generation of cell polarity and the cell fate decision. A central player in the Wnt signaling pathways is beta-catenin. Several studies have suggested that the Wnt/beta-catenin signaling pathway may be involved in the physiologic/pathologic control of thyroid cell growth and function. METHODS: We investigated the effect of thyroid-stimulating hormone (TSH) on the expression of Wnt proteins in FRTL-5 cells. To evaluate the effect of Wnt-1 on FRTL-5 cells growth, we isolated a stable cell line that overexpressed Wnt-1 (W1), and a vector-transfected cell clone (V3) was used as a control. We investigated the differences in the cellular growth rate, the cell cycle and cell apoptosis in the W1 and V3 cell lines. RESULTS: TSH caused a significant increase in the Wnt-1 level and a pronounced decrease in both the active and total beta-catenin levels in the FRTL-5 cells. The growth rate, the percentage of cells in the S/G2/M phase and the c-myc level were significantly higher in the W1 cells compared with the V3 cells. There was no change in the beta-catenin level and the cyclin D1 level in the W1 cells compared with the V3 cells. The cellular apoptosis induced by actinomycin-D seemed to be significantly decreased because the level of bcl-2 was increased in the W1 cells compared with the V3 cells. CONCLUSION: The FRTL-5 cells expressed Wnt-1 protein, and TSH increased the Wnt-1 expression, and it paradoxically decreased beta-catenin in the FRTL-5 cells. Overexpression of Wnt-1 in the FRTL-5 cells increased cell growth and it decreased apoptosis. Growth stimulation by Wnt-1 overexpression was not mediated by beta-catenin (the canonical Wnt pathway), but seemed to be mediated by activation of the Wnt/Ca2+ pathway, which involves an increased c-myc level. Suppression of apoptosis with Wnt-1 overexpression was due to the increased bcl-2 level.
Key Words: Beta-catenin, Thyroid, Wnt-1 protein


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