Proteomic analysis of PAX8 alterations provides new insights into its role as a master regulator of migration in high-grade serous ovarian cancer

High-grade serous ovarian cancer (HGSOC) is the most common subtype of ovarian cancer (1). This cancer is a heterogeneous disease associated with few shared genetic mutations (BRCA1, BRCA2, p53) (2) and with widely accepted origination from the fallopian tube epithelium (FTE). Eighty percent to 90% of HGSOCs, after malignant transformation, express the paired box transcription factor 8 (PAX8) (3). This transcriptional factor is normally expressed in the FTE but not in the healthy ovarian surface epithelium (OSE) (4). Several studies have recently reported PAX8 pivotal function in the migration, invasion and tumorigenic ability of ovarian cancer cells. Loss PAX8 in ovarian cancer cell lines decreases in vitro and in vivo tumor phenotype and promotes apoptosis (4-6). Hence, there is a growing interest to evaluate PAX8 not only as a diagnostic biomarker but also as a potential therapeutic target for HGSOC. However, the key pathways that allow PAX8 to regulate cellular processes in FTE and in HGSOC is still poorly understood.