Overexpression of EB1 in human esophageal squamous cell carcinoma (ESCC) may promote cellular growth by activating β-catenin/TCF pathway
Overexpression of EB1 in human esophageal squamous cell carcinoma (ESCC) may promote cellular growth by activating β-catenin/TCF pathway
Esophageal squamous cell carcinoma (ESCC) has a multifactorial etiology involving environmental and/or genetic factors. End-binding protein 1 (EB1), which was cloned as an interacting partner of the adenomatous polyposis coli (APC) tumor suppressor protein, was previously found overexpressed in ESCC. However, the precise role of EB1 in the development of this malignancy has not yet been elucidated. In this study, we analysed freshly resected ESCC specimens and demonstrated that EB1 was overexpressed in approximately 63% of tumor samples compared to matched normal tissue. We report that overexpression of EB1 in the ESCC line EC9706 significantly promotes cell growth, whereas suppression of EB1 protein level by RNA interference significantly inhibited growth of esophageal tumor cells. In addition, EB1 overexpression induced nuclear accumulation of β-catenin and promoted the transcriptional activity of β-catenin/T-cell factor (TCF). These effects were partially or completely abolished by coexpression of APC or ΔN TCF4, respectively. Also, we found that EB1 affected the interaction between β-catenin and APC. Furthermore, EB1 overexpression was correlated with cytoplasmic/nuclear accumulation of β-catenin in primary human ESCC. Taken together, these results support the novel hypothesis that EB1 overexpression may play a role in the development of ESCC by affecting APC function and activating the β-catenin/TCF pathway.
esophageal cancer, overexpression, EB1, APC, beta-catenin
6637-6645
Wang, Yihua
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Zhou, Xiaobo
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Zhu, Hongxia
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Liu, Shuang
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Zhou, Cuiqi
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Zhang, Guo
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Xue, Liyan
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Lu, Ning
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Quan, Lanping
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Bai, Jinfeng
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Zhan, Qimin
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Xu, Ningzhi
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6 October 2005
Wang, Yihua
f5044a95-60a7-42d2-87d6-5f1f789e3a7e
Zhou, Xiaobo
0deca180-bc8a-42d6-b6a6-237e04cae0e1
Zhu, Hongxia
34c74461-aab8-4886-8ed4-f80438fa2083
Liu, Shuang
f136b833-cd10-476d-80e2-8e8c69ee69bc
Zhou, Cuiqi
a79cddd5-12f5-41fd-af17-f553062f6d70
Zhang, Guo
7bce7bd5-04a3-48ac-8330-6f3521fab734
Xue, Liyan
d396faa2-726e-4672-aec4-7f56d9e186b0
Lu, Ning
8d60125f-c459-4a0e-8d87-c8e0123d40a5
Quan, Lanping
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Bai, Jinfeng
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Zhan, Qimin
c125182f-9a51-4062-93f0-9a30d98942f1
Xu, Ningzhi
7e2ddae3-ef56-4e9e-9ccb-4fddbcdf045f
Wang, Yihua, Zhou, Xiaobo, Zhu, Hongxia, Liu, Shuang, Zhou, Cuiqi, Zhang, Guo, Xue, Liyan, Lu, Ning, Quan, Lanping, Bai, Jinfeng, Zhan, Qimin and Xu, Ningzhi
(2005)
Overexpression of EB1 in human esophageal squamous cell carcinoma (ESCC) may promote cellular growth by activating β-catenin/TCF pathway.
Oncogene, 24 (44), .
(doi:10.1038/sj.onc.1208819).
(PMID:16007168)
Abstract
Esophageal squamous cell carcinoma (ESCC) has a multifactorial etiology involving environmental and/or genetic factors. End-binding protein 1 (EB1), which was cloned as an interacting partner of the adenomatous polyposis coli (APC) tumor suppressor protein, was previously found overexpressed in ESCC. However, the precise role of EB1 in the development of this malignancy has not yet been elucidated. In this study, we analysed freshly resected ESCC specimens and demonstrated that EB1 was overexpressed in approximately 63% of tumor samples compared to matched normal tissue. We report that overexpression of EB1 in the ESCC line EC9706 significantly promotes cell growth, whereas suppression of EB1 protein level by RNA interference significantly inhibited growth of esophageal tumor cells. In addition, EB1 overexpression induced nuclear accumulation of β-catenin and promoted the transcriptional activity of β-catenin/T-cell factor (TCF). These effects were partially or completely abolished by coexpression of APC or ΔN TCF4, respectively. Also, we found that EB1 affected the interaction between β-catenin and APC. Furthermore, EB1 overexpression was correlated with cytoplasmic/nuclear accumulation of β-catenin in primary human ESCC. Taken together, these results support the novel hypothesis that EB1 overexpression may play a role in the development of ESCC by affecting APC function and activating the β-catenin/TCF pathway.
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More information
Accepted/In Press date: 29 April 2005
e-pub ahead of print date: 20 June 2005
Published date: 6 October 2005
Keywords:
esophageal cancer, overexpression, EB1, APC, beta-catenin
Organisations:
Centre for Biological Sciences
Identifiers
Local EPrints ID: 385919
URI: http://eprints.soton.ac.uk/id/eprint/385919
ISSN: 0950-9232
PURE UUID: c57342df-3c2c-4800-8051-5f7286c2b7fc
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Date deposited: 26 Jan 2016 11:25
Last modified: 15 Mar 2024 03:52
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Contributors
Author:
Xiaobo Zhou
Author:
Hongxia Zhu
Author:
Shuang Liu
Author:
Cuiqi Zhou
Author:
Guo Zhang
Author:
Liyan Xue
Author:
Ning Lu
Author:
Lanping Quan
Author:
Jinfeng Bai
Author:
Qimin Zhan
Author:
Ningzhi Xu
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