Citations 1
The miR-362-3p/ BCLAF1 axis regulates cisplatin sensitivity and metastatic progression in triple-negative breast cancer
Liu, Zhaoji, Wu, Catherine, Uyemura, Madison M., Sardella, Barbara, Aronson, Emily K, Ke, Shizhong, Massicott, Erica S., Li, Xiaohui, Wang, Lin, Karagkouni, Dimitra, Kalavros, Nikolaos , Bogsan, Cristina S, Zhou, Lihan, Cheng, He, Garber, Judy E, Schnitt, Stuart J. , Tung, Nadine M, Heng, Yujing J., Heng, Yujing J. , Wu, C., Aronson, Emily K., Ke, Shizhong, Li, Xiaohui, Wang, Lin , Karagkouni, Dimitra , Vlachos, Ioannis S. , Batalini, Felipe , Bogsan, Cristina Stewart Bittencourt , Cheong, Jit Kong , Munson, Phillip B. , Mayer, Erica L. , Garber, Judy E. , Tung, Nadine , Kasinski, Andrea L. , Slack, Frank John , Wulf, Gerburg M.
No container title available | March 11, 2026 | Volume: No volume available | Issue: No issue available | Pages: No page available
Abstract Platinum-based chemotherapy remains a cornerstone of treatment for triple-negative breast cancer (TNBC), yet the molecular determinants governing platinum response remain poorly defined. By leveraging the randomized Phase II INFORM trial, which compared neoadjuvant cisplatin to anthracycline-based therapy in BRCA1/2 -mutant breast cancer—we identified miR-362-3p as a specific regulator of cisplatin sensitivity. Higher plasma miR-362-3p expression was exclusively associated with favorable clinical outcome in the cisplatin arm, with no association observed in the AC arm, decoupling platinum-specific vulnerability from general chemotherapy response. We used gain- and loss-of-function TNBC models to establish that miR-362-3p functions as a potent sensitizer to cisplatin in vitro and in vivo . Integrated TCGA analysis and experimental validation identified BCLAF1, a key regulator of DNA damage response, as a direct repression target of miR-362-3p. We uncovered a novel role for the miR-362-3p/ BCLAF1 axis in overcoming platinum resistance in TNBC.