Abstract
The epithelial-derived type II transmembrane serine protease epithin has been shown to be upregulated in a variety of cancer cell lines and tumor tissues, and its upregulation correlates well with tumor progression in many cases. However, little is known regarding the regulation of its expression and the mechanism of its roles in tumor progression. Here, we show that transforming growth factor-β (TGF-β), a potent inducer of epithelial-mesenchymal transition (EMT) in tumor progression, upregulates epithin, and that epithin plays a critical role in TGF-β-induced EMT. Forced overexpression of epithin induced EMT to exhibit characteristic morphological changes, alternations in EMT-related proteins and enhanced cell motility. Conversely, shRNA-mediated knockdown of endogenous epithin inhibited TGF-β-induced expression of mesenchymal markers and morphological changes. Furthermore, TGF-β-induced cell migration and invasion were significantly impaired by epithin knockdown. In addition, we demonstrate that TGF-β upregulates epithin transcriptionally via the Smad2/Smad4-mediated pathway. These results suggest that epithin is a key mediator of TGF-β-induced EMT in tumor progression.
| Original language | English |
|---|---|
| Pages (from-to) | 553-559 |
| Number of pages | 7 |
| Journal | Biochemical and Biophysical Research Communications |
| Volume | 395 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published - 2010 May 14 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Biochemistry
- Biophysics
- Cell Biology
- Molecular Biology
Cite this
Epithin, a target of transforming growth factor-β signaling, mediates epithelial-mesenchymal transition. / Lee, Hyo Seon; Kim, Chungho; Kim, Sang Bum; Kim, Moon Gyo; Park, Dongeun.
In: Biochemical and Biophysical Research Communications, Vol. 395, No. 4, 14.05.2010, p. 553-559.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Epithin, a target of transforming growth factor-β signaling, mediates epithelial-mesenchymal transition
AU - Lee, Hyo Seon
AU - Kim, Chungho
AU - Kim, Sang Bum
AU - Kim, Moon Gyo
AU - Park, Dongeun
PY - 2010/5/14
Y1 - 2010/5/14
N2 - The epithelial-derived type II transmembrane serine protease epithin has been shown to be upregulated in a variety of cancer cell lines and tumor tissues, and its upregulation correlates well with tumor progression in many cases. However, little is known regarding the regulation of its expression and the mechanism of its roles in tumor progression. Here, we show that transforming growth factor-β (TGF-β), a potent inducer of epithelial-mesenchymal transition (EMT) in tumor progression, upregulates epithin, and that epithin plays a critical role in TGF-β-induced EMT. Forced overexpression of epithin induced EMT to exhibit characteristic morphological changes, alternations in EMT-related proteins and enhanced cell motility. Conversely, shRNA-mediated knockdown of endogenous epithin inhibited TGF-β-induced expression of mesenchymal markers and morphological changes. Furthermore, TGF-β-induced cell migration and invasion were significantly impaired by epithin knockdown. In addition, we demonstrate that TGF-β upregulates epithin transcriptionally via the Smad2/Smad4-mediated pathway. These results suggest that epithin is a key mediator of TGF-β-induced EMT in tumor progression.
AB - The epithelial-derived type II transmembrane serine protease epithin has been shown to be upregulated in a variety of cancer cell lines and tumor tissues, and its upregulation correlates well with tumor progression in many cases. However, little is known regarding the regulation of its expression and the mechanism of its roles in tumor progression. Here, we show that transforming growth factor-β (TGF-β), a potent inducer of epithelial-mesenchymal transition (EMT) in tumor progression, upregulates epithin, and that epithin plays a critical role in TGF-β-induced EMT. Forced overexpression of epithin induced EMT to exhibit characteristic morphological changes, alternations in EMT-related proteins and enhanced cell motility. Conversely, shRNA-mediated knockdown of endogenous epithin inhibited TGF-β-induced expression of mesenchymal markers and morphological changes. Furthermore, TGF-β-induced cell migration and invasion were significantly impaired by epithin knockdown. In addition, we demonstrate that TGF-β upregulates epithin transcriptionally via the Smad2/Smad4-mediated pathway. These results suggest that epithin is a key mediator of TGF-β-induced EMT in tumor progression.
KW - Epithelial-mesenchymal transition
KW - Epithin
KW - TGF-β
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U2 - 10.1016/j.bbrc.2010.04.065
DO - 10.1016/j.bbrc.2010.04.065
M3 - Article
VL - 395
SP - 553
EP - 559
JO - The BMJ
JF - The BMJ
SN - 0730-6512
IS - 4
ER -