Back

The miR-362-3p/BCLAF1 axis regulates cisplatin sensitivity and metastatic progression in triple-negative breast cancer

Liu, Z.; Wu, C.; Uyemura, M.; Sardella, B. R.; Aronson, E. K.; Ke, S.; Massicott, E. S.; Li, X.; Wang, L.; Karagkouni, D.; Kalavros, N.; Vlachos, I. S.; Batalini, F.; Bogsan, C. S.; Cheong, J. K.; Zhou, L.; Cheng, H.; Munson, P.; Mayer, E. L.; Garber, J. E.; Schnitt, S. J.; Tung, N. M.; Kasinski, A. L.; Frank, S. J.; Wulf, G. M.; Heng, Y. J.

2026-03-10 oncology
10.64898/2026.03.09.26347941 medRxiv
Show 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.

Matching journals

The top 6 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.