Researchers at Duke University found that blocking a key enzyme not only kills multiple myeloma (MM) cancer cells but also boosts the effectiveness of existing therapies. MM is an incurable blood cancer, and drug resistance is an increasing problem.
The study, published in Blood, focused on ferroptosis, a natural form of cell death triggered by excess iron. MM cells suppress this process, allowing them to accumulate toxic levels of iron without dying. The researchers identified the enzyme kinase STK17B as the mechanism responsible for suppressing ferroptosis and regulating iron balance in MM cells. High levels of STK17B are linked to poor patient survival and drug resistance.
Using a specific inhibitor compound, the team was able to block STK17B, which reactivated ferroptosis and made the cancer cells more vulnerable to conventional MM treatments. When administered orally to MM mouse models, the inhibitor increased cancer cell iron uptake, induced ferroptosis, and significantly reduced tumor growth.
The researchers believe inhibiting STK17B holds great promise as a therapeutic strategy for multiple myeloma and plan to explore its potential to improve drug resistance in other cancers that also resist ferroptosis.