Clinical Value Screening, Prognostic Significance, and Key Gene Identification of TrkB in Laryngeal Carcinoma.

Abstract

Purpose Using human gene chip expression profiling technology to screen out downstream genes related to TrkB regulation in laryngeal cancer cells. Methods Using the Hep-2 TrkB shRNA cell line, divide it into an experimental group (shNTRK2) and a control group (PLKO1), and use the human gene expression microarray to screen out the differential genes. Then, select 10 upregulated genes and 10 downregulated genes from the differential genes, and use RT-PCR to verify whether the screening results of human gene expression microarray profiles are reliable. Use GO, KEGG, and miRNA enrichment analyses, PPI network diagram, etc., to analyze the differential genes and further screen out the key genes. Results A total of 318 differential genes (87 upregulated genes and 231 downregulated genes) were screened in laryngeal cancer cells. Use RT-PCR for the 10 upregulated differential genes (DMKN, FHL1, FOXN4, GGNBP1, HOXB9, ABCB1, TNFAI, RGS2, LINC01133, and FGG) and 10 downregulated differential genes (CHI3L1, FMOD, IGFBP1, IRF5, SPARC, NPAS4, TRPS1, TRAP, COL8A1, and DNER), and the results are consistent with the chip results, confirming the accuracy of the chip results; GO analysis results show that the downstream differential genes (DEGs) regulated by TrkB are mainly involved in biological processes such as retinol metabolic process, diterpenoid metabolic process, and regulation of cell-substrate adhesion. DEGs mainly affect cytoskeletal protein binding, serotonin-activated cation-selective channel activity, and sphingosine molecular functions. DEGs are mainly enriched in the cell periphery, secretory granule, cytoplasmic membrane-bounded vesicle lumen, blood microparticle, and other molecular components. The results of disease enrichment analysis show that the downstream differential genes regulated by TrkB are mainly involved in atypical hemolytic uremic syndrome, hematologic disease, meningococcal disease, lung cancer, susceptibility, asthma, and other diseases. The PPI network diagram results showed 7 hub genes, and then, we used GO analysis and KEGG enrichment analysis to see the biological process, cell component, molecular functions, and biological pathways. Conclusion Gene chip technology was used to screen out the differential genes of TrkB epigenetic modification in the Hep-2 cell line, and seven key genes (ALDH1A1, SDR16C5, PIK3R1, PLCG2, IL2RG, PIK3CD, and SPARC) were further screened using bioinformatics technology.