The tumor's fuel supply, essentially cut off
From within the very ecosystem that shelters cancer, University of Illinois Chicago researchers have drawn an unlikely ally: bacteria that colonize tumors. By studying the proteins these microbes produce, the team engineered a peptide called aurB that starves cancer cells of energy at the mitochondrial level, sidestepping a genetic limitation that had constrained earlier bacterial-inspired therapies. Tested in animal models of aggressive prostate cancer, aurB combined with radiation shrank tumors markedly — a finding that reframes the tumor microenvironment not merely as a fortress for disease, but as a potential pharmacy waiting to be explored.
- Hormone-resistant prostate cancer remains one of oncology's most stubborn challenges, and existing bacterial-inspired therapies were blocked by p53 mutations present in many patients — leaving a significant portion of sufferers without options.
- The UIC team cracked this barrier by targeting mitochondria directly: aurB binds to ATP synthase inside tumor cells, cutting off the energy supply that keeps cancer alive regardless of a patient's genetic profile.
- In mice, the combination of aurB and standard radiation produced striking tumor shrinkage with no apparent toxic side effects — even in bone metastasis models where cancer had already spread.
- The peptide has been patented and human clinical trials are now in preparation, signaling a rapid push from laboratory discovery toward potential clinical use.
- Researchers believe aurB is only the first find in what may be a vast, largely uncharted library of anti-cancer proteins produced by tumor-dwelling bacteria — suggesting the field is at an early frontier rather than a finishing line.
A research team at the University of Illinois Chicago has developed a new cancer therapy by turning to an unexpected source: the bacteria that naturally inhabit tumors. Their peptide, aurB, works by cutting off a cancer cell's energy supply — and when paired with radiation in animal models of prostate cancer, it shrank tumors dramatically.
The project grew from a question posed by associate professor Tohru Yamada: could the bacterial residents of tumors offer clues for drug design? His lab had previously built a therapy from a bacterial protein called a cupredoxin, which showed promise in brain cancer trials. The problem was dependency on p53, a tumor suppressor gene that is mutated — and mutated differently — across many patients, limiting who could benefit.
To find a p53-independent path, Yamada's team extracted tumor samples from breast cancer patients, sequenced the DNA of bacteria living inside them, and identified a cupredoxin protein called auracyanin. They synthesized a peptide mimicking it — aurB — and discovered it worked through a distinct mechanism: slipping into tumor cell mitochondria and binding to ATP synthase, the machinery that produces cellular energy. Disrupting this process effectively starved the tumor.
In mice engineered to develop hormone-resistant prostate cancer, the combination of aurB and radiation outperformed either treatment alone, with no apparent toxic side effects. Even in a bone metastasis model, tumor growth was substantially inhibited. The peptide has since been patented, and clinical trials are being planned.
Yamada sees aurB as a single discovery within what may be a much larger reservoir of bacterial proteins with anti-cancer potential. The tumor microenvironment — long understood as a landscape that helps cancer thrive — may, in his view, also hold the tools to dismantle it.
A team at the University of Illinois Chicago has engineered a new cancer treatment by borrowing from an unexpected source: bacteria that naturally live inside tumors. The therapy, a peptide called aurB, works by starving cancer cells of energy. When tested alongside radiation in animal models of prostate cancer, it shrank tumors dramatically—a result that suggests a fundamentally different way to attack the disease.
The discovery began with a simple observation. Scientists have known for years that bacteria colonize the tumor microenvironment, the tissue surrounding and within cancerous growths. Tohru Yamada, an associate professor in surgery and biomedical engineering at UIC, wondered whether these bacterial residents might offer clues for drug design. His lab had previously developed a peptide based on a bacterial protein called a cupredoxin, which showed promise in human trials for brain cancer. But that approach had a critical limitation: it only worked if a patient's tumor still carried a functioning p53 gene, a tumor suppressor that is mutated in many cancer patients. The mutations vary widely, meaning the drug would help some patients but not others.
Yamada's team set out to find a bacterial protein that could bypass p53 entirely. They extracted tumor samples from breast cancer patients, sequenced the DNA of bacteria living within them, and identified a cupredoxin protein called auracyanin. The researchers synthesized a peptide mimicking this protein and named it aurB. In the lab, aurB proved to work through a different mechanism: it slipped into tumor cell mitochondria—the cellular power plants—and bound to ATP synthase, the machinery that manufactures ATP, the energy currency all cells depend on. By disrupting this process, aurB essentially cut the tumor's fuel supply.
The real test came in animal models. The researchers used mice engineered to develop hormone-resistant prostate cancer, a particularly aggressive form of the disease. They gave some mice aurB alone, others radiation alone, and a third group received both treatments together. The combination was striking. Tumors in mice receiving aurB plus radiation shrank significantly compared to controls, with no apparent toxic side effects. The peptide amplified the effect of radiation, a standard treatment already used in prostate cancer care. In a bone metastasis model—simulating cancer that has spread to bone—the team saw substantial inhibition of tumor growth.
Yamada and his colleagues have already patented aurB and are now preparing to move toward human trials. But the researcher's vision extends further. He views auracyanin as merely one discovery in what he suspects is a vast library of bacterial proteins with anti-cancer potential. Many bacteria live in tumors; many of those bacteria produce proteins no one has yet examined for therapeutic use. The work suggests that the tumor microenvironment itself—long seen as a hostile ecosystem that helps cancer thrive—might be mined for the tools to fight it back.
Citas Notables
The mitochondria are the energy factories, and cancer cells need them to grow aggressively and rapidly. They would be an ideal target for cancer therapy.— Tohru Yamada, associate professor at UIC
There are many other bacterial proteins that could be sources of cancer drugs. We simply haven't tried them yet.— Tohru Yamada
La Conversación del Hearth Otra perspectiva de la historia
Why target the mitochondria instead of, say, the tumor's blood supply or its ability to hide from the immune system?
Because cancer cells are metabolic gluttons. They need energy constantly to grow and divide. The mitochondria are where that energy gets made. If you can shut that down, the tumor starves. It's a direct attack on what makes cancer cells different from normal cells.
But couldn't cancer cells just adapt? Evolve new ways to make energy?
That's a real question. The preclinical data is promising, but you're right—resistance is always a concern. That's partly why combining aurB with radiation matters. You're hitting the tumor from two angles at once, which makes adaptation harder.
The p53 angle is interesting. Why was that such a problem before?
P53 is a brake on cancer. Many tumors lose it or mutate it because losing the brake helps them grow faster. The previous bacterial peptide relied on p53 still being there to work. But in a lot of cancer patients, p53 is already broken. So you'd develop a drug that only helps some patients. aurB doesn't need p53 at all—it works through the mitochondria directly.
How did they know to look at bacteria in tumors in the first place?
Yamada's lab had already found one bacterial protein that worked against cancer. That success made them curious about what else might be hiding in the tumor microenvironment. It's a shift in thinking—instead of fighting the bacteria there, you ask what they might teach you.
What happens next?
Clinical trials. They need to test this in actual patients now, see if the preclinical results hold up. And Yamada thinks this is just the beginning—there are probably hundreds of bacterial proteins no one has looked at yet.