Transcriptomic Re-Analysis Reveals Inflammatory and Differentiation Pathway Changes in BRCA1-Deficient Ovarian Cancer Cells Following Ionizing Radiation

Publication Date

2026

Presentation Length

Poster/Gallery presentation

College

College of Sciences & Mathematics

Department

Psychological Sciences and Neurosciences, Department of

Faculty Mentor

Jinhee Park

Presentation Type

Article

Summary

Ovarian cancer associated with BRCA1 mutation is a serious disease with a high mortality rate. BRCA1 is a tumor suppressor gene that helps repair DNA damage. When BRCA1 does not function properly, DNA damage cannot be repaired, leading to an increase in mutations and a higher risk of tumor formation. Understanding these molecular changes is important for developing new treatments. In this study, we re-analyzed publicly available RNA-seq data to identify gene expression changes and affected biological pathways in BRCA1-mutant cancer cells. We compared BRCA1-null ovarian cancer cells (UWB) with cells in which normal BRCA1 function was restored (UWBBRCA1) after ionizing radiation-induced DNA damage. Using a false discovery rate (FDR) cutoff of 0.05, we identified 1,806 differentially expressed genes (DEGs), including 967 upregulated and 839 downregulated genes in BRCA1-null cells compared to BRCA1-restored cells following radiation treatment. Upregulated genes in BRCA1-null cancer cells were mainly involved in extracellular matrix organization and immune activation, suggesting increased tissue remodeling and inflammation. Some genes, such as IL6, IL1A, and CD40, indicate increased immune activity around the tumor. Downregulated genes in BRCA1-null cancer cells were associated with neuronal development, growth factor signaling, and cell differentiation. Genes such as NOTCH3, WNT5A, and SMAD play important roles in regulating cell fate and tissue organization. Their reduced expression suggests that normal cell development is suppressed, which may lead to uncontrolled cell growth. Overall, these results suggest that BRCA1 loss leads to increased inflammation and reduced cell differentiation, contributing to tumor progression. Based on this, targeting these abnormal signaling pathways could be a potential way to slow or kill BRCA1-null cancer cells.

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