From Defense to Disease: How the Immune System Fuels Epithelial-Mesenchymal Transition in Ovarian Cancer

Ovarian cancer is one of the most deadly gynecological cancers, with over 300 thousand new cases per year, most of which are diagnosed in advanced stages. The limited availability of effective biomarkers and lack of characteristic symptoms make early diagnosis difficult, resulting in a five-year survival rate of 30-40%. Mutations in the BRCA1 and BRCA2 genes and abnormalities of signaling pathways such as PI3K/AKT and TP53 play a key role in the progression of ovarian cancer. The immune system, which can act against tumors, often supports tumor development in the ovarian cancer microenvironment through immunoevasion, which is influenced by cytokines such as IL-6, IL-10, and TGF-β. Epithelial-to-mesenchymal transition (EMT) allows cancer cells to acquire mesenchymal characteristics, increasing their invasiveness and metastatic capacity. Immunological factors, including pro-inflammatory cytokines and signals from the tumor microenvironment regulate the EMT process. This review aims to present the role of EMT in ovarian cancer progression, its interactions with the immune system, and potential biomarkers and therapeutic targets. Modulation of the immune response and inhibition of EMT may constitute the basis for personalized therapies, which opens new possibilities for improving the prognosis and efficacy of treatment in patients with ovarian cancer.