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Abstract

C-X-C Motif Chemokine Ligand 6: A Preoperative Biomarker for Recurrent Glioblastoma Multiforme

Author(s): Lei Cheng*, X. D. Li, S. B. Wang, J. M. Yang and Yimu Fan
Department of Neurosurgery, Tianjin Huanhu Hospital, Jinnan, Tianjin 300350, 1Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China

Correspondence Address:
Lei Cheng, Department of Neurosurgery, Tianjin Huanhu Hospital, Jinnan, Tianjin 300350, China, E-mail: petre1000@163.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.

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