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Interferons are supposed to help the immune system fight cancer — but linger too long, and they flip the script. Salk Institute researchers uncovered a pathway where chronic interferon exposure disrupts mitochondria, triggering a chain reaction that suppresses immunity and helps tumors grow. Blocking a key molecule in this pathway reversed immunotherapy resistance in 9 out of 10 mice.
Interferons are the immune system's early-warning proteins — they sound the alarm when cancer appears and recruit immune cells to attack. But a new study from the Salk Institute, published in Science, reveals a troubling twist: when interferons stick around too long, they can actually help tumors grow instead of shrink them.
The research team found that chronic exposure to interferon II disrupts mitochondrial function in melanoma cells, causing mitochondrial RNA to leak out of the mitochondria. The cell misreads this as a threat, triggering a cascade that boosts levels of prostaglandin E2 — a molecule that suppresses the immune system and shields tumors from attack. When researchers blocked prostaglandin E2 production in mouse melanoma cells, the immune system regained its ability to recognize and destroy cancer — and tumors that were previously resistant to anti-PD1 immunotherapy completely regressed.
By the numbers:
Why it matters: Immunotherapy resistance is one of oncology's biggest unsolved problems. This discovery identifies a specific, targetable pathway that could help more patients benefit from existing immunotherapies — a potentially major step forward for cancer treatment.
