Key genes affecting the progression of nasopharyngeal carcinoma identified by RNA-sequencing and bioinformatic analysis

Aging (Albany NY). 2021 Sep 20;13(18):22176-22187. doi: 10.18632/aging.203521. Epub 2021 Sep 20.

Abstract

Background: The present work was conducted to screen the potential biomarkers affecting nasopharyngeal carcinoma (NPC) progression through RNA-sequencing (RNA-seq), bioinformatic analysis and functional experiments.

Materials and methods: Six normal samples and five NPC clinical samples were collected for RNA-seq analysis. The expression levels in both groups were determined through student's t-test. We identified genes of P < 0.01 as the differentially expressed genes (DEGs). In addition, gene set enrichment analysis (GSEA) was conducted. Afterwards, STRING V10 database was employed to extract protein interactions among the DEGs. Later, we established a protein-protein interaction (PPI) network, and used the Cytoscape software for network visualization. qRT-PCR was conducted to verify hub genes from clinical samples. Then, the function of CXCL10 in cell proliferation, apoptosis, invasion and migration was evaluated.

Results: A total of 2024 DEGs were identified, among which, 1449 were down-regulated and 575 were up-regulated. The PPI was constructed, and the hub genes including Insulin Like Growth Factor 1 (IGF1), C-X-C Motif Chemokine Ligand 10 (CXCL10), Interleukin 13 (IL13), Intercellular Adhesion Molecule 1 (ICAM1), G Protein Subunit Gamma Transducin 1 (GNGT1), Matrix Metallopeptidase 1 (MMP1), Neurexin 1 (NRXN1) and Matrix Metallopeptidase 3 (MMP3) were obtained. The expression levels of CXCL10, IGF1, MMP3, MMP1, ICAM1, and IL-13 were significantly up-regulated in tumor tissues. High expression levels of CXCL10, MMP3 and ICAM1 predicted poor prognosis of NPC patients. CXCL10 silencing suppressed NPC cell proliferation and migration.

Conclusions: CXCL10 may serve as a potential key gene affecting NPC genesis and progression.

Keywords: differentially expressed genes; nasopharyngeal carcinoma; progression; protein encoding genes; protein-protein interaction network.