Cephalochromin

Triple-negative breast cancer (TNBC) is an aggressive subtype characterized by the absence of estrogen, progesterone, and HER2 receptors, limiting treatment options due to the lack of targeted therapies. Survivin (BIRC5), an inhibitor of apoptosis (IAP) protein, is overexpressed in TNBC and contributes to tumor progression, chemoresistance, and poor prognosis. Cephalochromin, a fungal-derived bioactive compound, has demonstrated cytotoxic activity in various cancer models; however, its effects on breast cancer remain unexplored. In this study, we evaluated the antineoplastic potential of cephalochromin in breast cancer cells, focusing on its impact on cell viability, apoptosis, cell cycle regulation, and survivin modulation. Cephalochromin exhibited potent cytotoxic effects in TNBC models, inducing apoptosis, disrupting cell cycle progression, and downregulating survivin expression. Mechanistically, cephalochromin treatment induced PARP1 cleavage and increased the expression of γH2AX, SQSTM1/p62, and LC3BII. Gene expression analysis revealed the broad modulation of key regulators involved in apoptosis, DNA damage response, and macroautophagy. Furthermore, cephalochromin enhanced the cytotoxicity of paclitaxel and doxorubicin, showing additive synergistic interactions. In conclusion, our study provides compelling evidence of cephalochromin's antineoplastic activity in breast cancer, highlighting its potential to improve treatment outcomes. Further preclinical studies are warranted to validate their therapeutic efficacy and safety.