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Abstract

Basal-like breast cancer (BLBC) poses significant challenges due to its aggressive behavior and limited treatment options. Recent investigations have uncovered a promising avenue for addressing BLBC through the modulation of the FOXO1-KLF5 transcriptional axis by DNA damage chemotherapeutic drugs. In this study, BLBC cell lines were exposed to platinum-based compounds and anthracyclines to explore the impact on the FOXO1-KLF5 axis [1]. Activation of FOXO1 by DNA damage led to direct binding to the KLF5 promoter, resulting in the down-regulation of KLF5 expression. Consequently, suppressed BLBC cell viability and proliferation were observed. These findings shed light on a novel mechanism by which DNA damage-inducing agents exert their anti-tumor effects, providing insights into potential targeted therapies and combination treatments for BLBC. Further research into this axis holds promise for innovative strategies to combat this aggressive subtype of breast cancer and improve patient outcomes [2].