<p>Ovarian cancer (OC) presents a formidable public health challenge, characterized by rising incidence rates and high mortality. NRF3 (NFE2L3), a cap 'n' collar transcription factor, plays a complex role in the pathogenesis of various diseases, including cancer tumorigenesis and progression. Its regulatory mechanisms, including post-translational modifications and interactions with other transcription factors, are crucial for understanding its impact on cancer biology. A thorough examination of existing literature categorizes upstream and downstream genes, molecules, pathways, and mechanisms associated with NRF3, emphasizing its intricate roles and molecular actions in OC. NRF3 exhibits a dual role as a potential tumor suppressor or oncogene, depending on the cellular context and tumor microenvironment. Evidence from a comprehensive literature search and bioinformatics investigation reveals a pan-cancer link between NRF3 and key processes such as chemoresistance, immune evasion, and metastasis, with elevated expression correlating with poor survival outcomes in OC. Its oncogenic mechanisms within the tumor microenvironment highlight immunosuppressive roles that may compromise therapy responses, underscoring its potential as a theranostic biomarker in OC. Emerging evidence suggests that targeting NRF3 may offer novel therapeutic strategies, potentially enhancing treatment outcomes through combination therapies and immunotherapeutic approaches. Our review emphasizes the necessity for further translational research to validate NRF3 as a therapeutic target and biomarker, aiming to improve patient stratification and treatment efficacy in OC. Ultimately, understanding NRF3's multifaceted roles may pave the way for innovative, personalized treatment strategies that address the unique challenges posed by OC.</p>