前列腺癌（PCa）是一种广泛的全球健康问题，其特点是发病率升高，需要新的治疗靶点来改善患者的治疗效果。 FOXS1 与不同的癌症密切相关，但其在 PCa 中的功能仍不清楚。通过利用公共数据的生物信息学分析，研究了 FOXS1 的表达、其预后作用、PCa 中的临床意义以及 FOXS1 影响 PCa 进展的潜在机制。使用蛋白质印迹、免疫组织化学和 qRT-PCR 等多种方法评估临床 PCa 样本中的 FOXS1 和 HILPDA 水平。为了研究 FOXS1 在 PCa 中的功能和分子机制，采用了 CCK-8 测定、流式细胞术、伤口愈合测定、Transwell 测定和 Co-IP 测定等实验技术的组合。 PCa 中 FOXS1 表达水平显着升高，与肿瘤侵袭性和不良预后密切相关。调节FOXS1的表达，无论是上调还是下调，都会相应增强或抑制PCa细胞的生长、迁移和侵袭能力。从机制上讲，我们检测到 FOXS1 和 HILPDA 之间的直接相互作用，导致 FAK/PI3K/AKT 通路激活并促进 PCa 细胞中的 EMT。 FOXS1 与 HILPDA 合作启动 EMT，从而通过 FAK/PI3K/AKT 通路激活促进 PCa 进展。© 2024 美国实验生物学会联合会。

Prostate cancer (PCa) is a widespread global health concern characterized by elevated rates of occurrence, and there is a need for novel therapeutic targets to enhance patient outcomes. FOXS1 is closely linked to different cancers, but its function in PCa is still unknown. The expression of FOXS1, its prognostic role, clinical significance in PCa, and the potential mechanism by which FOXS1 affects PCa progression were investigated through bioinformatics analysis utilizing public data. The levels of FOXS1 and HILPDA were evaluated in clinical PCa samples using various methods, such as western blotting, immunohistochemistry, and qRT-PCR. To examine the function and molecular mechanisms of FOXS1 in PCa, a combination of experimental techniques including CCK-8 assay, flow cytometry, wound-healing assay, Transwell assay, and Co-IP assay were employed. The FOXS1 expression levels were significantly raised in PCa, correlating strongly with tumor aggressiveness and an unfavorable prognosis. Regulating FOXS1 expression, whether upregulating or downregulating it, correspondingly enhanced or inhibited the growth, migration, and invasion capabilities of PCa cells. Mechanistically, we detected a direct interaction between FOXS1 and HILPDA, resulting in the pathway activation of FAK/PI3K/AKT and facilitation EMT in PCa cells. FOXS1 collaborates with HILPDA to initiate EMT, thereby facilitating the PCa progression through the FAK/PI3K/AKT pathway activation.© 2024 Federation of American Societies for Experimental Biology.