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Influence of vascular endothelial growth factor and radiation on gap junctional intercellular communication in glioblastoma multiforme cell lines

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Neural Regeneration Research 2017年第11期12卷 1816-1822页

作者： reinhardt krcek Pauline Latzer Irenaus Anton Adamietz Helmut Biihler Carsten Theiss Institute of Anatomy Department of CytologyRuhr-University BochumBochumNorth Rhine-WestphaliaGermany Department of Radiotherapy and Radio-Oncology University Medical Centre MarienhospitalRuhr-University BochumHerneNorth Rhine-WestphaliaGermany Institute for Molecular Oncology Radio-Biology and Experimental RadiotherapyUniversity Medical Centre MarienhospitalRuhr-University BochumHerneNorth Rhine-WestphaliaGermany

Glioblastoma multiforme （GBM） is a highly aggressive glial brain tumor with an unfavorable prognosis despite all current therapies including surgery, radiation and chemotherapy. One characteristic of this tumor is a strong synthesis of vascular endothelial growth factor （VEGF）, an angiogenesis factor, followed by pronounced vascularization. VEGF became a target in the treatment of GBM, for example with bevacizumab or the tyrosine kinase inhibitor axitinib, which blocks VEGF receptors. To improve patients＇ prognosis, new targets in the treatment of GBM are under investigations. The role of gap junctions in GBM remains un- known, but some experimental therapies affect these intercellular channels to treat the tumor. Gap junctions are composed of connexins to allow the transport of small molecules between adjacent cells through gap junc- tional intercellular communication （GJIC）. Based on data derived from astrocytes in former studies, which show that VEGF is able to enhance GJIC, the current study analyzed the effects of VEGF, radiation therapy and VEGF receptor blockade by axitinib on GJIC in human GBM cell lines U-87 and U-251. While VEGF is able to induce GJIC in U-251 cells but not in U-87 cells, radiation enhances GJIC in both cell lines. VEGF reocptor blockade by axitinib diminishes radiation induced effects in U-251 partially, while increases GJIC in U-87 cells. Our data indicate that VEGF and radiation are both modifying components of GJ1C in pathologic brain tumor tissue.

关键词： cell communication vascular endothelial growth factor irradiation vascular endothelial growth factor-receptor blockade glioma neurobiotin connexin cell culture immunohistochemistry microinjection

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