Results: Mic60 silencing led to significant upregulation of EMT-associated transcription factors, including Zeb2, Lbx1, Snail, Twist1, accompanied by increased Ncadherin and Vimentin expression and decreased E-cadherin levels.NF-B signaling was also activated upon Mic60 loss.In vivo, Mic60 depletion resulted in faster tumor growth and increased tumor weight, indicating a pronounced effect on tumor aggressiveness.Conclusions: These findings demonstrate that Mic60 loss drives a more aggressive breast cancer phenotype, characterized by activation of EMT-and NF-B-related pathways, increased migratory and invasive potential, and accelerated tumor growth in vivo.Mic60 loss thus acts as a key driver of BC aggressiveness and highlights Mic60-associated pathways as potential targets for prognostic and therapeutic strategies in aggressive BC.
Building similarity graph...
Analyzing shared references across papers
Loading...
M. Rotxes Costa
F. Opdam
M. Vlasov
Vall d'Hebron Institut de Recerca
ESMO Open
Karolinska Institutet
The University of Texas MD Anderson Cancer Center
Institut Gustave Roussy
Building similarity graph...
Analyzing shared references across papers
Loading...
Costa et al. (Wed,) studied this question.
synapsesocial.com/papers/69d0ae68659487ece0fa45ce — DOI: https://doi.org/10.1016/j.esmoop.2026.106294