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. 2012 Nov 26;154(1):25–35. doi: 10.1210/en.2012-1728

Fig. 5.

Fig. 5.

Stable reexpression of TRβ in the FTC-236 thyroid cancer cells reduces cell proliferation and migration by attenuating β-catenin signaling. A, Western blot analysis of expression of TRβ in stable cells after transfection of control (Neo) or THRB-expressing vector in FTC-236 cells. B, Cell proliferation was lower in TRβ-expressing FTC-236 cells (TRβ9 and TRβ23) than in control FTC-236 cells (Neo1 and Neo4). Data are presented as mean ± se. **, P < 0.05; *, P < 0.01. C, Wound-healing assay showed that reexpressing of the TRβ inhibited cell migration of FTC-236 cells. Data are presented as mean ± se. *, P < 0.01. D, Western blot analysis of p-β-catenin (serine 552), total β-catenin, cyclin D1, and GAPDH in whole-cell lysates from TRβ-expressing FTC-236 cells and control FTC-236 cells. E, Quantification of relative protein abundance of p-β-catenin, total β-catenin, and cyclin D1 after normalization using GAPDH as a loading control. Data presented as mean ± se. #, P < 0.001. F, Western blot analysis of protein abundance of β-catenin and cyclin D1 in the nuclear and cytoplasm cell fractions. PARP was used as loading control for nuclear fraction, and α-tubulin was used as loading controls for cytoplasmic fraction from FTC-236 cells.