title: The effect of CXCR4 silencing on epithelial-mesenchymal transition related genes in glioma U87 cells.
abstract: The epithelial-mesenchymal transition (EMT) of tumor cells is deemed to be closely associated with tumor metastasis. CXCR4 has been proved to play an important role in the process of tumor metastasis. This study illustrates the function and expression of CXCR4 silencing and the EMT related genes in the human glioma cell line U87. The results showed that CXCR4 silencing could inhibit the cell invasive and adhesion potentials, expression of N-cadherin, vimentin, β-catenin, TGF-β1, p-Smad2, and p-Akt, and the activity of transcription factors NF-κB, AP-1, Snail, and twist. Meanwhile, CXCR4 silencing could also up-regulate the expression of E-cadherin, indicating that silencing of CXCR4 expression can inhibit the expression of EMT related genes in U87 cells. The study would provide a potential theoretical basis for the further exploration of the role of CXCR4 in human glioma.
authors.affiliation: Department of Clinical Laboratory, Tianjin Huan Hu Hospital, Tianjin, 300060, China; Tianjin Key Laboratory of Cerebral Vessels and Neural Degeneration, Tianjin, 300060, China.
authors.forename: Yu
authors.initials: Y
authors.lastname: Zhu
authors.forename: Ping
authors.initials: P
authors.lastname: Yang
authors.forename: Qin
authors.initials: Q
authors.lastname: Wang
authors.forename: Jingyi
authors.initials: J
authors.lastname: Hu
authors.forename: Jing
authors.initials: J
authors.lastname: Xue
authors.forename: Guo
authors.initials: G
authors.lastname: Li
authors.forename: Guodong
authors.initials: G
authors.lastname: Zhang
authors.forename: Xu
authors.initials: X
authors.lastname: Li
authors.forename: Wei
authors.initials: W
authors.lastname: Li
authors.forename: Chunlei
authors.initials: C
authors.lastname: Zhou
authors.forename: Meng
authors.initials: M
authors.lastname: Zhao
authors.forename: Dong
authors.initials: D
authors.lastname: Wang
mesh_terms: D015703:Antigens, CD / Q000235:genetics / Q000378:metabolism; D017209:Apoptosis; D015153:Blotting, Western; D015820:Cadherins / Q000235:genetics / Q000378:metabolism; D002448:Cell Adhesion; D002465:Cell Movement; D049109:Cell Proliferation; D004797:Enzyme-Linked Immunosorbent Assay; D058750:Epithelial-Mesenchymal Transition / Q000235:genetics*; D005910:Glioma / Q000235:genetics* / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism; D009687:Nuclear Proteins / Q000235:genetics / Q000378:metabolism; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics; D034741:RNA, Small Interfering / Q000235:genetics*; D060888:Real-Time Polymerase Chain Reaction; D019718:Receptors, CXCR4 / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D051899:Smad2 Protein / Q000235:genetics / Q000378:metabolism; D000071250:Snail Family Transcription Factors; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000235:genetics / Q000378:metabolism; D014407:Tumor Cells, Cultured; D051879:Twist-Related Protein 1 / Q000235:genetics / Q000378:metabolism; D014746:Vimentin / Q000235:genetics / Q000378:metabolism; D051176:beta Catenin / Q000235:genetics / Q000378:metabolism
chemical_list: D015703:Antigens, CD; C050361:CDH2 protein, human; C527276:CXCR4 protein, human; D015820:Cadherins; D016328:NF-kappa B; D009687:Nuclear Proteins; D012333:RNA, Messenger; D034741:RNA, Small Interfering; D019718:Receptors, CXCR4; C497782:SMAD2 protein, human; D051899:Smad2 Protein; D000071250:Snail Family Transcription Factors; C103173:TWIST1 protein, human; D014157:Transcription Factors; D053773:Transforming Growth Factor beta1; D051879:Twist-Related Protein 1; D014746:Vimentin; D051176:beta Catenin; D051057:Proto-Oncogene Proteins c-akt
keywords: CXCR4; epithelial-mesenchymal transition; glioma