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Hyun Chung Choi  (Choi HC) 1 Article
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
J Korean Endocr Soc. 2007;22(1):35-44.   Published online February 1, 2007
DOI: https://doi.org/10.3803/jkes.2007.22.1.35
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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.
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