Unveiling the prognostic value of ARID3A in breast cancer through bioinformatic analysis

通过生物信息学分析揭示ARID3A在乳腺癌中的预后价值

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作者:Wen-Run Cai, Xu-Gang Sun, Yue Yu, Xin Wang, Xu-Chen Cao, Xiao-Feng Liu

Conclusion

These findings indicate that ARID3A may serve as a prognostic biomarker and therapeutic target in breast cancer, providing insights into its involvement in oncogenic pathways and interactions, particularly with TP53, that may drive cancer development and progression.

Methods

ARID3A mRNA and protein expression levels were analyzed using UALCAN, GEPIA databases, and immunohistochemistry from our hospital samples. Clinical prognostic parameters and survival data were examined through bioinformatics tools, including GEPIA, Bc-GenExMiner, and BEST. Subtype-specific expression and co-expression, particularly with REXO1, were evaluated using LinkedOmics, TIMER, and bc-GenExMiner. Functional enrichment analysis was conducted via LinkedOmics. Protein-protein interactions (PPI) were established using GeneMANIA and STRING, with validation through molecular docking using Cluspro.

Objective

Identifying reliable prognostic markers for breast cancer is crucial for improving survival rates and reducing mortality. Recent studies highlight the AT-rich interactive domain-containing protein (ARID) family, particularly ARID3A, as influential in cancer progression, though its specific role in breast cancer remains unclear. This study investigates ARID3A's expression, prognostic relevance, clinicopathological correlations, co-expression profiles, and protein-protein interactions in breast cancer.

Results

Elevated ARID3A expression was associated with poor prognosis in breast cancer, particularly in Luminal and HER2-positive subtypes. A positive correlation with REXO1 was identified, and enrichment analysis emphasized ARID3A's involvement in immune-related pathways, such as "interferon gamma production" and "primary immunodeficiency." PPI network and docking studies identified TP53 as a potential binding partner, suggesting a novel interaction influencing tumor progression.

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