Study on the mechanism of BGN in progression and metastasis of ccRCC

Abstract

Abstract Purpose To investigate the role of BGN in the progression and metastasis of ccRCC. Methods Based on multiple public databases, we investigated the expression level of BGN in ccRCC, its clinical significance, and its association with immune cells. Real-time fluorescence quantitative PCR was employed to validate BGN expression in tumor and adjacent normal tissues. BGN knockdown cells were generated through lentiviral transfection to examine the impact of BGN on ccRCC. Cell proliferation, migration, and invasion were assessed using wound healing, transwell migration, and invasion assays, respectively. Differential gene analysis, GO-KEGG analysis, and GSEA analysis were performed by RNA sequencing to elucidate the underlying signaling pathways . Results Our findings from database analysis and polymerase chain reaction (PCR) revealed a significant upregulation of BGN expression in kidney cancer tissues compared to normal tissues. Further analysis demonstrated a correlation between high BGN expression and ccRCC progression and immune infiltration. In vitro experiments confirmed that BGN silencing effectively inhibited cell proliferation, migration, and invasion of ccRCC. Mechanistically, these effects may be mediated through the MAPK signaling pathway . Conclusion BGN potentially plays a pivotal role in the progression and metastasis of ccRCC, possibly acting through the MAPK signaling pathway. Therefore, BGN holds promise as a potential therapeutic target for ccRCC.