Gene expression profile analysis of the bone microenvironment in patients with spinal metastases.

Abstract:

:The present study aimed to identify the underlying molecular mechanisms associated with spinal metastases. Gene expression profiles in cancellous bone samples from the spines of five patients with spinal metastases, with different primary cancers, and three normal control patients were measured using microarray analysis and subsequently compared. The differentially expressed genes (DEGs) identified were filtered using bioinformatics analyses followed by cluster analysis, gene ontology (GO) term and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses. Finally, a protein-protein interaction network was constructed and analyzed. A total of 152 upregulated and 388 downregulated DEGs were identified. The cluster analysis demonstrated a marked difference between the gene expression profiles of samples from patients with spinal metastases and those from normal patients. The GO terms enriched in the upregulated DEGs were associated with cell death, and those enriched in the downregulated DEGs were associated with the cell cycle. The upregulated DEGs were enriched in signaling pathways associated with tight junctions, and the downregulated DEGs were enriched in signaling pathways associated with porphyrin metabolism. In the PPI network constructed, transcription factor AP-1 and proliferating cell nuclear antigen had the highest connectivity degrees with the upregulated and downregulated DEGs, respectively. The gene expression profile data from the present study provides new insights into the underlying molecular mechanisms of spinal metastases, and will aid in the development of novel anticancer treatments.

journal_name

Oncol Lett

journal_title

Oncology letters

authors

Liu W,Liang Y,Bian C,Jiang L,Zheng G,Dong J

doi

10.3892/ol.2017.7267

subject

Has Abstract

pub_date

2018-01-01 00:00:00

pages

61-68

issue

1

eissn

1792-1074

issn

1792-1082

pii

OL-0-0-7267

journal_volume

15

pub_type

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