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.
journal_name
Int J Oncoljournal_title
International journal of oncologyauthors
Xu Q,Tan Y,Zhang K,Li Ydoi
10.3892/ijo.2013.2026subject
Has Abstractpub_date
2013-10-01 00:00:00pages
1187-93issue
4eissn
1019-6439issn
1791-2423journal_volume
43pub_type
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