Background: Ovarian cancer (OC) has high mortality and relapse rates, yet the contribution of the noncoding genome to these outcomes remains poorly understood. Enhancer RNAs (eRNAs) are frequently altered in OC, but the origins and functional relevance of these changes are unclear. We expect noncoding mutations within enhancers to alter eRNA expression and sequence, disrupting their post-transcriptional functions. We integrate whole genome noncoding mutations, eRNA expression and eRNA-mRNA interactions to prioritise regulatory variants and affected post-transcriptional processes. eRNA’s impact on target mRNA stability and translation efficiency allow further refinement to resolve associated gene expression changes. Whole-genome and transcriptome data from 241 OC patients (TCGA) were analysed alongside our curated post-transcriptional eRNA–mRNA interactions (Benova et al., 2025a, bioRxiv). We further developed TranCi, a method for prioritising functional noncoding mutations using the eRNA post-transcriptional interactome (Benova et al., 2025b, bioRxiv). Candidate mutation-eRNA pairs were validated via siRNA knockdown of eRNAs, and assays for proliferation, migration, and angiogenesis. TranCi identified 912 regulatory mutations, including 17 recurrent high-confidence mutations linked to 16 eRNAs and 119 target genes. Over 95% of these genes are essential in OC (DepMap) or significantly dysregulated in tumours. One mutation reduces en76310, a cytoplasmic polyA-enriched eRNA whose targets regulate cytoskeletal remodelling and metastasis. siRNA depletion in OVCAR3 cells reduced migration, increased target mRNA, and suppressed endothelial pro-angiogenic activity in co-culture assays. These results demonstrate that our integrative framework detects functional enhancer noncoding mutations, and en76310 validation confirms it captures regulatory changes affecting OC biology.