Objective: The mechanisms underlying the progression from endometriosis to Endometriosis-Associated Ovarian Cancer (EAOC) are poorly understood. Our study aimed to explore the role of NLRP3 inflammasome activation during the progression of endometriosis to EAOC. Method: The clinical tissue samples of endometriosis and EAOC endometrium were collected with normal endometrium served as controls. Immuno-histochemical staining was performed to determine the expression patterns of NLRP3, caspase-1 and IL-1β, as well as BRCC3, an upstream regulator of NLRP3. The association of NLRP3 level with the clinical parameters in EAOC patients was analyzed. Furthermore, the functional role of BRCC3 in endometriosis malignant transformation into EAOC was explored using MTT, colony formation, flow cytometric, and transwell assays. Results: Our study showed that activation of NLRP3 inflammasome occurred in EAOC and endometriosis samples compared to the normal endometrium. NLRP3 expression was also positively correlated with FIGO stage, and negatively associated with tumor differentiation. Moreover, BRCC3 was significantly increased in EAOC and endometriosis, positively correlated with to NLRP3 in EAOC tissues. Functionally, our study demonstrated that BRCC3 over-expression significantly promoted cell proliferation, inhibited apoptosis, and enhanced migration and invasion of endometriosis cells. Conversely, knockdown of BRCC3 suppressed such effects in endometriosis cells. Mechanically, BRCC3 activated NLRP3 expression, and NLRP3 knockdown reversed the effects of BRCC3 on endometriosis cells. Conclusion: In conclusion, BRCC3 could regulate NLRP3 expression, thereby inducing malignant transformation of endometriosis to EAOC.