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Ovarian cancer is currently treated with surgery and chemotherapy. Chemotherapy for ovarian cancer is based on drugs that act on any cell that is rapidly dividing, healthy or malignant, which has side effects. Baylor College of Medicine researchers and the University of Texas MD Anderson Cancer Center have revealed a previously unknown cellular pathway that selectively regulates a mutant protein-p53-R175H, linked to ovarian cancer growth.
They identified a key regulator of this pathway—USP15—and suggest that designing drugs directed at this regulator might lead to better ways to control cancer growth. Serious ovarian carcinomas-the most lethal and common form of ovarian cancer have mutations in the p53 gene. These mutations play key roles in the production of tumors and in the development of drug resistance.
Normal p53 is rapidly broken down in some healthy cells, but p53 mutants such as p53-R175H, are not. They form very stable protein clusters in cells that promote cancer and induce drug resistance. If the mutant are remorem from p53 forms from cancer cells, the cells will enter a path toward cell death and become more sensitive to chemotherapy.
The researchers discovered that MCB613 does not decrease the levels of mutant p53-R175H protein directly. It reduces the levels of another protein- USP15 that removes a specific tag from the p53 mutant that targets it to undergo degradation inside cells. Fewer molecules of USP15, results in more mutant p53-R175H protein tagged for degradation in the cell.
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