Elevated SLC4A11 expression promotes OV progression via interaction with EGFR.

Ovarian cancer (OV) is one of the most prevalent and lethal gynecological malignancies worldwide, often diagnosed at advanced stages due to its asymptomatic early progression. Despite standard treatments, including tumor reduction surgery and platinum-based chemotherapy, the majority of patients face high risks of recurrence and metastasis, underscoring the need for a deeper understanding of the molecular mechanisms driving OV progression. This study focused on Solute Carrier Family 4 Member 11 (SLC4A11), a gene highly expressed in OV, to explore its functional role and underlying mechanisms. Analysis of public datasets (TCGA and GEO) revealed that SLC4A11 expression was significantly elevated in OV tissues compared to normal tissues and was associated with poorer overall survival and advanced clinical stages. Functional in vitro assays, including colony formation, migration, and CCK-8 experiments, demonstrated that SLC4A11 overexpression enhanced OV cell proliferation and migration, while its knockdown inhibited these processes. In vivo studies using a subcutaneous xenograft mouse model further validated the role of SLC4A11 in promoting tumor growth. Mechanistically, SLC4A11 was found to directly interact with the Epidermal growth factor receptor (EGFR), activating the PI3K/AKT signaling pathway, a critical driver of cancer progression. These findings highlight SLC4A11 as a key regulator of OV development and a potential therapeutic target, offering new insights for improving treatment strategies and patient outcomes in ovarian cancer.