Comprehensive analysis of bioinformatics and system biology reveals the association between Girdin and hepatocellular carcinoma
Introduction: Hepatocellular carcinoma stands as the most common cause of global cancer-related mortality. The actin-binding protein Girdin exhibits elevated expression in diverse tumors, fostering tumorigenesis and progression. Nevertheless, the precise mechanism by which Girdin regulates liver cancer remains elusive. Methods: This study comprehensively analyzed the expression level of Girdin in liver cancer and adjacent tissue, along with the correlation between Girdin expression and the clinical characteristics and prognosis of liver cancer. The analysis involved the integration of data from The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), Clinical Proteomic Tumor Analysis Consortium (CPTAC) database, and immunohistochemistry. Subsequently, the expression level of Girdin was knocked down to elucidate its role in the progression of liver cancer. Transcriptome sequencing was employed to investigate the mechanistic underpinnings of Girdin's regulatory impact on liver cancer. Additionally, the Comparative Toxicogenomics Database (CTD) was utilized to identify potential drugs or molecules for liver cancer treatment. Results: The findings revealed elevated Girdin expression in liver cancer tissues, and heightened Girdin expression correlated with adverse clinical features and prognosis. Silencing of Girdin markedly impeded the proliferation and migration of hepatocellular carcinoma cells. Moreover, transcriptome sequencing demonstrated that silencing Girdin led to differential expression of 176 genes and inhibition of the PI3K/Akt signaling pathway. Ultimately, we propose that Imatinib Mesylate, Orantinib, Resveratrol, Sorafenib, and Curcumin mayinteract with Girdin, potentially contributing to the treatment of liver cancer. Conclusion: This study reveals the association between Girdin and hepatocellular carcinoma, providing novel clues for future research and treatment of hepatocellular carcinoma. Overall design: HepG2 cells were divided into 2 groups, including the negative control group (si-NC) and the si-Girdin group. RNA-seq was conducted.