An established risk factor for ovarian cancer is obesity; epidemiological data show that obese women have a higher incidence and a lower survival rate. PubMed, Scopus, Web of Science, and Google Scholar were searched for pertinent material published between 2010 and 2026 for this narrative review. Reviews, clinical trials, and peer-reviewed research on obesity, ovarian cancer, PI3K/AKT/mTOR, leptin-JAK/STAT3, NF-κB, and associated treatments were included; duplicates and irrelevant publications were eliminated. The pathogenic connection results from adipokine dysregulation, metabolic changes that encourage carcinogenesis, and persistent low-grade inflammation brought on by obesity. Via cytokines, growth factors, and free fatty acids, excess adiposity triggers pro-oncogenic pathways, including PI3K/AKT/mTOR, leptin-JAK/STAT, and NF-κB. Proliferation, angiogenesis, metastasis, and chemoresistance are all fueled by these mechanisms. Through energy provision and extracellular matrix remodeling, adipocyte–tumor interaction in the omentum further increases the likelihood of metastasis. Clinical trials have shown varying degrees of success for pharmacological therapies that target these pathways, including NF-κB modulators, JAK inhibitors, and mTOR inhibitors. Curcumin, oridonin, and genistein are examples of natural substances that show preclinical potential in modifying these signaling cascades. Calorie restriction, low-starch diets, and organized exercise are examples of lifestyle modifications that can enhance metabolic profiles and perhaps affect prognosis. Molecular profiling in precision medicine techniques may improve focused treatment and get past resistance. This study highlights the necessity of multi-modal interventions to address the obesity–ovarian cancer nexus by integrating molecular knowledge, therapeutic techniques, and lifestyle factors.
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