Crosstalk between p38 and Smad3 through TGF-β1 in JEG-3 choriocarcinoma cells

Xu,Qian; Tan,Yusi; Zhang,Kongyan; Li,Yuhong

doi:10.3892/ijo.2013.2026

Crosstalk between p38 and Smad3 through TGF-β1 in JEG-3 choriocarcinoma cells

Authors:
- Qian Xu
- Yusi Tan
- Kongyan Zhang
- Yuhong Li
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Affiliations: Department of Basic Medicine, Chengde Medical College, Chengde, Hebei 067000, P.R. China
Published online on: July 22, 2013 https://doi.org/10.3892/ijo.2013.2026
Pages: 1187-1193

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Abstract

Choriocarcinoma is a highly malignant trophoblastic tumor related to pregnancy that often occurs with a complete hydatidiform mole. It grows quickly and can also widely metastasize to other organs or tissues through both the venous and lymphatic systems. The transforming growth factor-β1 (TGF-β1) belongs to a growth factor superfamily and has been suggested to play a critical role in regulating the genesis and development of choriocarcinoma through a variety of Smad-independent pathways, including the p38 MAPK pathway. Previous studies indicated that TGF-β can activate the p38 MAPK pathway. In this study, we investigated Smad and p38 MAPK signaling in JEG-3 choriocarcinoma cells using p38 MAPK inhibitor and TGF-β receptor inhibitor. Immunofluorescence and western blot assays were used to detect the proteins in Smad and p38 MAPK pathways. Our data demonstrated that TGF-β can activate Smad3 and induce Smad3 translocation into the nucleus in JEG-3 cells. Blockade of the TGF-β pathway significantly reduced the expression levels of p38 and phospho-p38. p38 MAPK inhibitors (SB 203580) can attenuate TGF-β1-induced Smad3 expression and suppress the activation of smad3. These findings indicate crosstalk between p38 and smad3 through TGF-β1 in choriocarcinoma cells.

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