LITAF suppresses breast cancer and paclitaxel resistance by ubiquitinating and degrading PCMT1 to inhibit COX-2-dependent arachidonic acid metabolism

Background: Paclitaxel (PTX) is a first-line chemotherapeutic agent extensively employed in the management of breast cancer (BC); however, the emergence of drug resistance frequently results in unsatisfactory clinical outcomes and poor prognosis. This study aimed to investigate the pathogenic mechanisms that drive PTX resistance in BC. Methods: , nude mice were used to explore the effect of LITAF on tumor response to PTX treatment. Results: . Conclusion: LITAF regulates the ubiquitination-mediated degradation of PCMT1 to inhibit COX-2-dependent AA metabolism, thereby enhancing the sensitivity of BC cells to PTX and providing a potential therapeutic strategy to overcome PTX resistance in BC.