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Mol Carcinog. 2009 Mar;48(3):212-219. doi: 10.1002/mc.20471.

EB1 acts as an oncogene via activating beta-catenin/TCF pathway to promote cellular growth and inhibit apoptosis.

Author information

1
Laboratory of Cell and Molecular Biology, Cancer Institute & Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, PR China.
2
Department of Pathology, Ohio State University, Columbus, Ohio.
3
Signal Transduction Laboratory, London Research Institute, Lincoln's Inn Fields Laboratories, Cancer Research UK (CR-UK), London, UK.

Abstract

Previously we showed that end-binding protein 1 (EB1) may promote cellular growth by activating beta-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 beta-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 DeltaN TCF4, an inhibitor of beta-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 beta-catenin/TCF pathway to promote cellular growth and inhibit apoptosis.

PMID:
18680107
DOI:
10.1002/mc.20471
[Indexed for MEDLINE]

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