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.
Bruun et al. (Wed,) studied this question.
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