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Ovarian cancer is the most aggressive gynecological tumor and poses a severe threat to the life and health of women worldwide. In recent years, a variety of novel targeted therapies have been successively developed and introduced into clinical practice. Although the mortality rate of ovarian cancer has been partially controlled, the 5-year survival rate of patients remains at approximately 50%. Multiple factors contribute to the persistently high mortality of ovarian cancer: the disease presents occult clinical manifestations at the early stage, and there is a lack of early screening biomarkers with both high sensitivity and specificity verified by large-sample clinical trials; additionally, tumor recurrence is frequent and chemotherapy resistance is prevalent. Conventional in vitro models such as cell lines fail to recapitulate the prominent heterogeneity of ovarian cancer and tend to undergo substantial genomic drift during long-term passaging. Patient-derived xenograft (PDX) models remedy some of these deficiencies, yet they still suffer from drawbacks including low establishment success rates, long experimental cycles, and the inability to simulate in vivo immune responses. Furthermore, safety regulations and ethical constraints on clinical trials hinder the research and development of candidate new drugs, and numerous findings from basic research cannot be translated into clinical practice. Faced with the above research bottlenecks, the emergence of organoid technology provides a stable and reliable in vitro platform for investigating the basic mechanisms and translational medicine of ovarian cancer. Ovarian cancer is a highly heterogeneous tumor with diverse pathological subtypes, and distinct subtypes exhibit markedly different clinical phenotypes and molecular features. Even within the same pathological subtype, significant heterogeneity exists among different patients and across different regions of a single tumor, which serves as a key cause of treatment failure and drug resistance in ovarian cancer. The organoid system can effectively recapitulate inter-tumoral and intra-tumoral heterogeneity. Organoid models established from patients’ tumor tissues enable rapid in vitro drug screening and facilitate research on individualized therapeutic strategies. The formation of various ovarian cancer subtypes results from the synergistic effects of multiple genetic alterations. The combination of gene-editing technology and organoid platforms helps uncover the regulatory roles of genetic abnormalities in the initiation and malignant progression of ovarian cancer.