“You can’t just rip out a receptor that does useful work everywhere in the body,” said Erick M. Carreira, co-leader of the research at ETH Zürich. That blunt statement captures the central dilemma his team faced.
The glucocorticoid receptor helps cancer cells hide by pushing them into a dormant, drug-resistant state. But the same protein also calms inflammation throughout the body.
Destroy it globally, and you cause real harm. The solution, built by Carreira and Katharina Gapp, is a molecule that only destroys that receptor when a specific color of light hits it. No light, no work.
Shine the right wavelength, and the molecule, called a photoPROTAC, goes after the receptor inside the tumor. Keep the light off, and the molecule stays inert, leaving the rest of the body alone.
Cancer’s dirty trick is well known to oncologists. Tumor cells can slip into biological hibernation. They shrug off treatment, lie low, and wait for conditions to improve.
Then they wake up and bring the disease back. For decades, researchers have tried to shut down this hiding strategy without causing serious harm elsewhere. The photoPROTAC approach is a direct response to that failure.
The work appears in the journal Proceedings of the National Academy of Sciences. Carreira and Gapp engineered a class of molecules that are drug-like compounds.
They are not drugs yet. They are tools to probe a question: can you disrupt the hibernation switch in a tumor without poisoning the patient? The glucocorticoid receptor sits inside cells and reacts to stress hormones.
When it switches on in certain solid tumors, such as lung cancer, it pushes the cells into a dormant state. That state is drug-resistant.
The obvious fix would be to destroy the receptor outright. But the catch is that the same receptor does important jobs all over the body, including calming inflammation. Removing it everywhere would cause real damage.
What was needed was a way to hit the receptor inside a tumor and leave the rest of the body alone. That is what the team set out to build. Their solution is a class of molecules called photoPROTACs.
Shine the right light on them, and they go to work. Keep the light off, and they remain inert.
The researchers are careful not to overstate what they have. These are not yet human therapies. They are molecular tools that allow scientists to ask a precise question: what happens if you destroy the glucocorticoid receptor only in a tumor, and only when you want to?
The answer, if it works in living animals and eventually in people, could change how certain cancers are treated. What is at stake here is the ability to probe, and possibly disrupt, the dormant state that makes some cancers so hard to cure.
The photoPROTACs give researchers a switch. They can turn the destruction of the receptor on and off with light. That kind of control is new.
It lets scientists study the biology of tumor dormancy in a way that was not possible before. Carreira and Gapp are based in Zurich. Their work is early, but it addresses a problem that has frustrated cancer researchers for decades.
The hibernation strategy used by tumor cells is one of the most evasive in all of oncology. This molecule is a step toward a way to wake those sleeping cells up and make them killable again.
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