Scientists found something useful hiding inside the tumors. Not just cells, but bacteria. And now we know one of them produces a compound that starves cancer.
It works on prostate cancer models. Really well, actually. Especially when mixed with radiation.
The trick? Cutting off the energy supply.
“The mitochondria are very important for a cellsurvive; they are the energy factories,” says Tohru Yamada.
Cancer cells are greedy. They need massive amounts of fuel to grow fast. That makes their mitochondria a perfect weak spot. A target.
The p53 Problem
For years we knew tumors were full of microbes. The tumor microenvironment isn’t just empty space; it’s crowded with bacteria. Researchers recently started wondering if we could borrow something from these hitchhikers.
Yamada’s team already found one. A protein called cupredoxin. It suppresses tumor growth by moving electrons around.
They even put it in clinical trials. For adults with various cancers and kids with brain cancer.
But here is the catch. The old drug only worked if the p53 gene was functional.
Bad luck.
p53 gets mutated a lot in cancer patients. Mutations vary from person to person. So the treatment helped some and ignored others. Ineffective half the time? No one likes that.
“We wanted to have an anti cancer agent that doesn’t use p53 function,” Yamada noted.
So they looked elsewhere.
Hunting for a New Protein
The search was specific. They needed a bacterial protein that targets mitochondria directly. Skip p53 entirely.
They looked at breast cancer samples. Sequenced the DNA inside. Found bacteria living there.
One species stood out. It contained auracyanin. Another cupredoxin protein doing similar heavy lifting to the old one but through a different door.
They stripped down auracyanin to its essentials. Created a small fragment called aurB.
Here is how aurB operates.
- It slips into the mitochondria of tumor cells
- It attaches to ATP synthase
- It jams the machine
ATP is the fuel cells use to do anything. AurB turns off the engine. No ATP. No growth. Dead end for the tumor.
Prostate Cancer Gets Sliced
Did it work in mice?
Yes. And not just in any mice.
The team used models lacking active p53. These were tough cases. The kind that usually shrug off other treatments.
They added radiation therapy. The standard for prostate cancer.
The combination hit hard.
Tumor growth stalled. Significant reduction. No major toxicity signs.
“The combination significantly enhanced the activity,” Yamada said.
They tested it on tibial bone metastasis too. The tumors shrank. Preclinically promising doesn’t really capture it. It was striking.
Why does radiation make it better?
Maybe the stress of radiation weakens the cells further, making the energy blockade even more effective. Or maybe it’s just synergy.
Patenting the Path
UIC has the patent. Office of Technology Management handled it.
Next step? Human trials.
Yamada isn’t stopping here though.
Auracyanin might be the first. There are thousands of other bacterial proteins in those tumors. Untested. Unmapped.
“We simply haven’t tried them yet,” he said.
Countless opportunities sitting in the trash bin of the tumor microenvironment. Waiting for someone to dig.
Collaborators from UI Health helped. Surgeons like Martin Borhani, Aslam Ejaza, Ajay Rana Enrico Benedetti, and Tapas K Das Gupta brought the surgical expertise. Engineering minds from the College of Engineering joined in. Dr. Samer Naffouje and others from Medicine too.
A mixed crew.
Maybe that is what we need. Bacteria, doctors, engineers all working together because the old way was running out of steam.
Or maybe this is just another lead that dies in the clinic.
Time will tell. But the tumors gave up a secret.
