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Published in: Journal of Experimental & Clinical Cancer Research 1/2011

Open Access 01-12-2011 | Research

More expressions of BDNF and TrkB in multiple hepatocellular carcinoma and anti-BDNF or K252a induced apoptosis, supressed invasion of HepG2 and HCCLM3 cells

Authors: Dawei Guo, Xuezhong Hou, Hongbin Zhang, Wenyu Sun, Lei Zhu, Jian Liang, Xiaofeng Jiang

Published in: Journal of Experimental & Clinical Cancer Research | Issue 1/2011

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Abstract

Background

Brain-derived neurotrophic factor (BDNF) and its receptor Tropomysin-related kinase B (TrkB) are commonly up-regulated in a variety of human tumors. However, the roles of BDNF/TrkB in hepatocellular carcinoma (HCC) have been poorly investigated.

Methods

We evaluated the expressions of BDNF and TrkB in 65 cases of HCC by immunohistochemical staining. Moreover, in human HCC cell lines of HepG2 and high metastatic HCCLM3, the secretory BDNF in supernatant was measured by ELISA, the effects of BDNF neutralizing antibody or Trk tyrosine kinase inhibitor K252a on apoptosis and invasion were examined by flow cytometry and transwell assay respectively.

Results

Higher expression of BDNF (63.1%) or positive expression of TrkB (55.4%) was found in HCC specimens, which was significantly correlated with multiple and advanced stage of HCC. BDNF secretory level in HCCLM3 was higher than that in HepG2 cells. Both anti-BDNF and K252a effectively induced apoptosis and suppressed invasion of HepG2 and HCCLM3 cells.

Conclusions

These findings suggested that BDNF/TrkB are essential for HCC cells survival and invasion. BDNF/TrkB signaling should probably be an effective target to prevent HCC advancement.
Appendix
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Metadata
Title
More expressions of BDNF and TrkB in multiple hepatocellular carcinoma and anti-BDNF or K252a induced apoptosis, supressed invasion of HepG2 and HCCLM3 cells
Authors
Dawei Guo
Xuezhong Hou
Hongbin Zhang
Wenyu Sun
Lei Zhu
Jian Liang
Xiaofeng Jiang
Publication date
01-12-2011
Publisher
BioMed Central
Published in
Journal of Experimental & Clinical Cancer Research / Issue 1/2011
Electronic ISSN: 1756-9966
DOI
https://doi.org/10.1186/1756-9966-30-97

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