Background
Colorectal cancer (CRC) is one of the most malignant cancer worldwide, which leads to a high incidence and mortality. The molecular mechanism in CRC is still limited. The
Conclusions
These findings regarded TTI1 as a vital promoting factor in CRC development and provided a potential biomarker for CRC treatment.
Methods
The expression dataset (GSE44076) was downloaded from Gene Expression Omnibus (GEO) and differentially expressed genes (DEGs) analysis was done using R 'limma' packages. Weighted gene co-expression network analysis (WGCNA) was done and tumor-specific modules were picked up for Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. The hub gene was selected with higher inter-connectivity. Expression levels of TTI1 were verified by in clinical CRC tissues. The cell counting kit-8 (CCK-8) assay was to measure the proliferative ability of TTI1.
Results
Eight hundred and eight up-regulated and 929 down-regulated DEGs were screened out. Up-regulated genes enriched in cell proliferation and down-regulated genes enriched in oxidation-reduction process. After WGCNA, the yellow module was found to be the most significant tumor-specific module. Function analysis showed genes in the yellow module enriched in oxidation-reduction, cell proliferation and extracellular matrix (ECM)-receptor interaction. TTI1 was demonstrated as the hub gene. Real-time quantitative reverse transcription((qRT-PCR) results showed TTI1 significantly expressed higher in CRC tissues than adjacent normal tissues. TTI1 dramatically correlated with proliferation in CRC. Conclusions: These findings regarded TTI1 as a vital promoting factor in CRC development and provided a potential biomarker for CRC treatment.