SNX1 inhibits human ovarian cancer progression via regulation of the cell cycle, apoptosis and migration

Sorting nexin 1 (SNX1), a member of the sorting nexin family, has been implicated in various cellular processes, yet its role in ovarian Cancer (OV) remains poorly characterized. In this study, we systematically investigated the expression pattern, prognostic relevance and functional impact of SNX1 in OV. Bioinformatics analysis revealed that SNX1 is significantly downregulated in OV tissues, and its low expression is associated with poor overall and progression-free survival. Gene set enrichment analysis indicated that SNX1 downregulation is linked to activation of cancer-related pathways, including p53 signaling, PI3K/Akt signaling, and cell cycle-associated programs such as E2F targets and G2/M checkpoint. Functionally, SNX1 overexpression inhibited OV cell proliferation, blocked G1/S transition (with downregulation of E2F1, CDK2, CDK6, and cyclin D1), promoted Apoptosis, and suppressed cell migration by modulating EMT markers (upregulating E-cadherin; downregulating N-cadherin, vimentin, Snail1, and β-catenin). Drug sensitivity analysis demonstrated a synergistic anti-tumor effect between SNX1 overexpression and paclitaxel treatment. Collectively, our findings identify SNX1 as a tumor suppressor and potential therapeutic target in OV, functioning through regulation of cell cycle, Apoptosis and migration.

SNX1; drug sensitivity; epithelial-mesenchymal transition; ovarian cancer; paclitaxel.