Cross-link regulation of precursor N-cadherin and FGFR1 by GDNF increases U251MG cell viability

Tang,Chuan-Xi; Gu,Yan-Xia; Liu,Xin-Feng; Tong,Shu-Yan; Ayanlaja,Abiola A.; Gao,Yue; Ji,Guang-Quan; Xiong,Ye; Huang,Lin-Yan; Gao,Dian-Shuai

doi:10.3892/or.2018.6405

Cross-link regulation of precursor N-cadherin and FGFR1 by GDNF increases U251MG cell viability

Authors:
- Chuan-Xi Tang
- Yan-Xia Gu
- Xin-Feng Liu
- Shu-Yan Tong
- Abiola A. Ayanlaja
- Yue Gao
- Guang-Quan Ji
- Ye Xiong
- Lin-Yan Huang
- Dian-Shuai Gao
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Affiliations: Department of Neurobiology and Anatomy, Xuzhou Key Laboratory of Neurobiology, Xuzhou Medical University, Xuzhou, Jiangsu 221000, P.R. China, School of Nursing, Xuzhou Medical University, Xuzhou, Jiangsu 221000, P.R. China, Department of Neurology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu 221000, P.R. China, School of Medical Technology, Xuzhou Medical University, Xuzhou, Jiangsu 221000, P.R. China
Published online on: April 30, 2018 https://doi.org/10.3892/or.2018.6405
Pages: 443-453

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Abstract

Glial cell line-derived neurotrophic factor (GDNF) is considered to be involved in the development of glioma. However, uncovering the underlying mechanism of the proliferation of glioma cells is a challenging work in progress. We have identified the binding of the precursor of N-cadherin (proN-cadherin) and GDNF on the cell membrane in previous studies. In the present study, we observed increased U251 Malignant glioma (U251MG) cell viability by exogenous GDNF (50 ng/ml). We also confirmed that the high expression of the proN-cadherin was stimulated by exogenous GDNF. Concurrently, we affirmed that lower expression of proN-cadherin correlated with reduced glioma cell viability. Additionally, we observed glioma cell U251MG viability as the phosphorylation level of FGFR1 at Y653 and Y654 was increased after exogenous GDNF treatment, which led to increased interaction between proN-cadherin and FGFR1 (pY653+Y654). Our experiments presented a new mechanism adopted by GDNF supporting glioma development and indicated a possible therapeutic potential via the inhibition of proN-cadherin/FGFR1 interaction.

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