EB1 acts as an oncogene via activating β-catenin/TCF pathway to promote cellular growth and inhibit apoptosis
✍ Scribed by Mei Liu; Shangbin Yang; Yihua Wang; Hongxia Zhu; Shuang Yan; Wei Zhang; Lanping Quan; Jinfeng Bai; Ningzhi Xu
- Book ID
- 102504661
- Publisher
- John Wiley and Sons
- Year
- 2008
- Tongue
- English
- Weight
- 244 KB
- Volume
- 48
- Category
- Article
- ISSN
- 0899-1987
- DOI
- 10.1002/mc.20471
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✦ Synopsis
Abstract
Previously we showed that end‐binding protein 1 (EB1) may promote cellular growth by activating β‐catenin/T‐cell factor (TCF) pathway. To further investigate the role of EB1 in regulating cellular growth, we established an EB1‐inducible expression system in which the protein level of EB1 was significantly upregulated upon doxycycline induction. We found that EB1 promoted cellular growth and resulted in a significant increase in colony formation. In addition, EB1 could induce tumor formation in nude mice, activate β‐catenin‐dependent gene expression and upregulate the transcriptional activity of c‐myc. We also showed that EB1 in this manner inhibited apoptosis of 293‐T‐REx cells upon cisplatin and upregulated expression of Bcl‐2, whereas ΔN TCF4, an inhibitor of β‐catenin/TCF pathway, could completely or partially abolish the effects of EB1 on the promotion of cell growth and the inhibition of apoptosis activity. Moreover, knockdown of c‐myc by RNAi could abrogate upregulation of EB1‐dependent induction of Bcl‐2 expression. Overall, EB1 acts as a potential oncogene via activating β‐catenin/TCF pathway to promote cellular growth and inhibit apoptosis. © 2008 Wiley‐Liss, Inc.