WK peptide-guided copper nanozyme disrupts redox balance, suppresses triple-negative breast cancer

Current treatments for aggressive breast cancer, particularly the triple-negative subtype (TNBC), face significant limitations due to drug resistance and systemic toxicity. These challenges highlight an urgent need for innovative therapeutic strategies. Targeting the redox balance within tumor cells presents a promising avenue, as cancer cells often exhibit altered redox homeostasis, making them vulnerable to interventions that disrupt this delicate equilibrium. This study explores a nanozyme approach to address these critical gaps.

This study developed a novel WK peptide-guided copper-based nanozyme designed to target tumor lesions. The nanozyme's functional properties were evaluated for its peroxidase-like activity and its ability to deplete glutathione. Researchers conducted both in vitro and in vivo experiments to assess the nanozyme's mechanistic effects on breast cancer cells. Key endpoints included the induction of ROS burst, inhibition of the PI3K-AKT-mTOR signaling pathway, and the triggering of apoptosis, ultimately measuring its impact on tumor suppression.

The developed nanozyme demonstrated a potent dual mechanism for disrupting cancer cell redox homeostasis. It exhibited significant peroxidase-like activity, effectively converting endogenous hydrogen peroxide into cytotoxic radicals within tumor cells. Concurrently, the nanozyme was shown to deplete glutathione, further exacerbating oxidative stress. In both in vitro and in vivo experiments, the nanozyme effectively induced a substantial ROS burst in breast cancer cells. This cellular stress led to the inhibition of the crucial PI3K-AKT-mTOR signaling pathway, a key regulator of cell growth and survival. Ultimately, these actions triggered apoptosis, resulting in significant tumor suppression.

The WK peptide-guided copper nanozyme effectively induces a ROS burst, inhibits the PI3K-AKT-mTOR pathway, and triggers apoptosis, leading to significant tumor suppression in breast cancer models.