作者: Yu-Xiao Liu , Jun-Nian Zhou , Ke-Hui Liu , Xiang-pin Fu , Zhi-Wen Zhang
DOI: 10.2147/CMAR.S191249
关键词: Cell migration 、 Glioma 、 Proteomics 、 Ectopic expression 、 Immunoprecipitation 、 Microarray analysis techniques 、 Chemistry 、 Transport protein 、 Cancer research 、 Cell adhesion
摘要: Purpose A better understanding of the underlying molecular mechanisms in treatment failure bevacizumab (BEV) for malignant glioma would contribute to overcome therapeutic resistance. Methods Here, we used a quantitative proteomic method identify signatures glioblastoma cell after BEV by two-dimensional liquid chromatography-tandem mass spectrometry analysis and 6-plex iTRAQ quantification. Next, function cold-inducible RNA-binding protein (CIRP), one most significantly affected proteins drug treatment, was evaluated resistance cells invasion assays animal xenograft assays. Target molecules bound CIRP were determined using immunoprecipitation microarray analysis. Then, these mRNAs identified real-time PCR. Results Eighty-seven with significant fold changes. The biological functional indicated that involved process cellular signal transduction, adhesion, transport. expression greatly decreased ectopic abolished migration BEV-treated cells. In addition, could bind mRNA CXCL12 inhibit BEV-induced increase Conclusion These data suggested may take part gliomas binding migration-relative RNAs.