Oncogenic role of C11orf86 in ovarian cancer involving hypoxia response and immune modulation

Ovarian cancer is often diagnosed at advanced stages and lacks effective biomarkers for prognosis prediction or targeted therapy. The biological role of C11orf86, a previously uncharacterized gene, remains unclear in ovarian cancer. C11orf86 expression and clinical relevance were analyzed using transcriptomic datasets from TCGA, GTEx, and patient tissues. Functional assays, including siRNA knockdown, overexpression, qPCR, Western blotting, flow cytometry, and Transwell assays, were performed in SKOV3 ovarian cancer cells. Pathway enrichment and immune correlation analyses were conducted using publicly available online databases. C11orf86 was significantly upregulated in ovarian cancer and associated with poor prognosis, particularly in the TP53-mutant subgroup. Immunohistochemistry confirmed elevated expression of C11orf86 in primary and metastatic ovarian cancer tissues. Functionally, C11orf86 promoted proliferation, migration, invasion, and cell cycle progression of ovarian cancer cells. It was induced by hypoxia and HIF-1α overexpression, while its silencing was accompanied by reduced STAT3 phosphorylation and HIF-1α levels. C11orf86-correlated genes were enriched in cell cycle, hypoxia, and immune-related pathways. Furthermore, C11orf86 expression showed strong correlation with Th2 infiltration and key Th2 markers including STAT5A. C11orf86 promotes malignant behaviors in ovarian cancer and may be associated with Th2-related immune features. It is linked to the STAT3-HIF-1α axis and may serve as a promising prognostic biomarker and potential therapeutic target.