Northwestern Medicine researchers have discovered that PRMT5 plays a crucial role in chemotherapy resistance in advanced ovarian cancer, a significant cause of cancer-related deaths among women. Despite advancements in treatment, many patients experience recurrence and resistance. The study reveals the regulatory relationship between KEAP1 and PRMT5, where resistance disrupts KEAP1's function, resulting in increased PRMT5 levels. This protein heightens stress response gene activity, thereby supporting drug resistance. Combining PRMT5 inhibitors with chemotherapy drugs may enhance treatment efficacy, offering new avenues in the fight against this challenging cancer.
Chemotherapy resistance is the biggest clinical challenge for physicians to treat this type of cancer. Initially, it's very sensitive, but quickly it becomes chemoresistant.
We need to figure out how the cells become chemoresistant, why they're becoming chemoresistant and what kind of molecular mechanisms are enabling these cells to survive under harsh chemo treatments.
The protein KEAP1 is a key regulator of PRMT5. Under normal conditions, KEAP1 binds to PRMT5 and initiates its degradation, maintaining balanced protein levels.
PRMT5 influences the activity of stress response genes, fostering a cellular environment that supports drug resistance.
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