SPOCK2 promotes the invasion and migration of ovarian cancer cells through FAK signaling pathway.

Abstract

Objective: Ovarian cancer is one of the most prevalent malignancies worldwide, with the highest mortality rate among gynecological cancers. This study aims to investigate the molecular mechanisms of SPOCK2 in ovarian cancer progression and metastasis and evaluate its potential as a therapeutic target.

Methods: The expression levels of SPOCK2 in ovarian cancer tissues and normal tissues were analyzed using data from The Cancer Genome Atlas (TCGA) and immunohistochemistry experiments. Functional assays, including epithelial-mesenchymal transition (EMT), invasion, and migration assays, were performed in high-grade serous ovarian cancer (HGSOC) cells to explore the role of SPOCK2. The interaction between SPOCK2 and ITGA3 and the subsequent activation of focal adhesion kinase (FAK) signaling were investigated. In vivo experiments were conducted to validate the effects of SPOCK2 knockdown on tumor metastasis and invasiveness.

Results: SPOCK2 expression was significantly upregulated in ovarian cancer tissues compared to normal tissues and was associated with poor prognosis. Functional assays demonstrated that SPOCK2 promotes EMT, invasion, and migration in HGSOC cells by interacting with ITGA3 and activating FAK signaling. In vivo experiments confirmed that SPOCK2 knockdown significantly suppressed tumor metastasis and invasiveness.

Conclusion: This study highlights the critical role of the SPOCK2/ITGA3 axis in driving ovarian cancer progression and provides evidence for SPOCK2 as a potential molecular marker and therapeutic target. These findings offer new insights into the early diagnosis and treatment of ovarian cancer, with significant clinical implications for improving patient outcomes.