Introduction: Testis expressed gene 11 (TEX11) is a X-linked gene and mainly involved in meiotic arrest and male infertility, its role in the testicular germ cell tumor (TGCT) remains unknown. Thus, we aim to investigate the role of TEX11 in the pathogenesis of TGCT.
Methods: In this study, the overexpression plasmid of TEX11 (pcDNA-3.1+/TEX11) was constructed and transfected into NCCIT cell and Tcam-2 cell respectively. After transfection, the change of cell function was detected, including cell cycle, proliferation and apoptosis, migration and invasion. Furthermore, RNA sequence was used to investigated the gene expression profile alternation after TEX11 over-expression in Tcam-2 cell, genes with P value = 0.05 and |log2FC| = 1 were considered as differentially expressed genes (DEGs). GO and KEGG enrichment analyses were used to revealed the function of TEX11.
Results: The results showed that after overexpressed TEX11 in NCCIT and Tcam-2, its mRNA expression level was significantly increased. The Transwell indicated that TEX11 inhibited the migration and invasion ability of both NCCIT and Tcam-2 cells. Furthermore, the bioinformatics analysis showed that a total of 131 DEGs were detected in the sequence data, including 75 up-regulated DEGs and 56 down-regulated DEGs. The GO analysis showed that the down-regulated DEGs were significantly enriched in cellular process, biological regulation, protein binding, cell and cell part. KEGG pathway analysis revealed that these genes were mainly enriched in cell adhesion molecules (CAMs), ovarian steroidogenesis, NF-kappa B pathway and leukocyte transendothelial migration. Based on the phenotype change of migration and invasion ability, we chosen the differentially expressed gene ITGB2 from CAMs pathway, as a target gene. Using GEPIA database, we found that ITGB2 was significantly up-regulated in the TGCT tissue, and negatively related with the expression level of TEX11.
Conclusions: In conclusion, we believed that TEX11 is a novel gene in the pathogenesis of TGCT. TEX11 may down-regulate ITGB2 gene through cell adhesion molecules pathway, thereby inhibit the invasion and migration ability of testicular germ cell tumor.
Source of Funding: The work was supported by Graduate Independent Innovation Project Fund of Central South University (2020zzts229).