Bacteria living inside tumors are now the unlikely inspiration for a new cancer therapy. Researchers at the University of Illinois Chicago developed a peptide called aurB that targets cancer cells' mitochondria, cutting off their energy supply. In preclinical prostate cancer models, aurB combined with radiation significantly shrank tumors — and it works even when the commonly mutated p53 gene is inactive.
Bacteria living inside tumors are now the unlikely inspiration for a new cancer therapy. Researchers at the University of Illinois Chicago (UIC) developed a peptide called aurB, derived from a bacterial protein called auracyanin — a copper-containing protein found in bacteria identified within breast tumor samples. aurB works by entering cancer cell mitochondria and binding to ATP synthase, a key enzyme in energy production, effectively starving tumors of the fuel they need to grow.
What makes aurB especially notable is that it bypasses the p53 gene pathway — a critical advantage, since p53 is frequently mutated in cancer patients, limiting the effectiveness of many existing therapies. In preclinical studies using hormone therapy-resistant prostate cancer mouse models, aurB combined with radiation therapy produced significant tumor reduction without notable toxicity.
Key Takeaways:
Why it matters: Many cancer patients don't respond to therapies that rely on p53 function. A mitochondria-targeting, p53-independent approach like aurB could open new treatment avenues for patients with limited options — and the broader strategy of mining tumor bacteria for drug candidates may unlock an entirely new class of cancer therapies.
