C-X-C Motif Chemokine Ligand 6: A Preoperative Biomarker for Recurrent Glioblastoma Multiforme
Department of Neurosurgery, Tianjin Huanhu Hospital, Jinnan, Tianjin 300350, 1Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China
Lei Cheng, Department of Neurosurgery, Tianjin Huanhu Hospital, Jinnan, Tianjin 300350, China, E-mail: email@example.com
To explore the function of C-X-C motif chemokine ligand as a prospective early biomarker for recurrent glioblastoma multiforme is the objective of the study. The differentially expressed genes for glioblastoma multiforme patients were systematically explored; the gene ontology and Kyoto encyclopedia of genes and genomes enrichment analysis for potential hub gene was established; the functional network was developed by protein-protein interaction method. The glioblastoma multiforme cell line U251 was established for the in vitro functional experiments; the wound healing assay as well as transwell assay were conducted to measure tumor properties in U251 cells. The expression of C-X-C motif chemokine ligand 6 in recurrent patients of glioblastoma multiforme was significantly higher than in non-recurrent patients (p<0.05), suggesting C-X-C motif chemokine ligand 6 was an independent prognostic indicator for glioblastoma multiforme recurrence. Based on the gene ontology and Kyoto encyclopedia of genes and genomes enrichment analysis as well as a protein-protein interaction network for the C-X-C motif chemokine ligand 6, programmed death ligand-1 and signal transducer and activator of transcription 3 signaling were primarily associated with C-X-C motif chemokine ligand 6. C-X-C motif chemokine ligand 6 over-expression treatments induced markedly enhanced expression levels for programmed death ligand-1 and phospho-signal transducer and activator of transcription 3. At the same time, the regulation of C-X-C motif chemokine ligand 6 for U251 cells tumor properties was programmed death ligand-1 dependent since silencing of programmed death ligand-1 obviously attenuated the functions of C-X-C motif chemokine ligand 6 over-expression. Moreover, it could be implied that the expression levels of programmed death ligand-1 and phospho-signal transducer and activator of transcription 3 were linked to the recurrent status of glioblastoma multiforme patients, as their expression was remarkably accelerated for recurrent glioblastoma multiforme patients. This integrated study provided a potential biomarker and offered beneficial references for future clinical administration as well as evaluation of recurrent glioblastoma multiforme.