Researchers at UT Southwestern Medical Center have identified that the protein RIP1 could eventually inhibit the growth of aggressive malignant brain tumors including glioblastomas, astrocytomas, oligodendrogliomas and ependymomas. The finding was published online on August 22th in Cell Reports.
RIP1 plays a role as a cellular switch in brain tumor cells; by binding to the receptor EGFRvIII, RIP1 regulates survival and death of cancerous cells. The binding of RIP1 and EGFRvIII activates NFκB, which is important for the growth of tumor cells.
“Our study identifies a new mechanism involving RIP1 that regulates cell division and death in glioblastomas,” said senior author Dr. Amyn Habib, associate professor of neurology and neurotherapeutics at UT Southwestern, and staff neurologist at VA North Texas Health Care System. “For individuals with glioblastomas, this finding identified a target for the development of a drug treatment option that currently does not exist.”
In the study, researchers used an animal model to examine the interaction of RIP1 and EGFRvIII. When RIP1 is switched off in the model, NFκB and following signaling processes were stopped too, leading to cancer cells being diverted into a self-destruct mode.
According to the American Cancer Society, about 30% of brain tumors are gliomas, a fast-growing, treatment-resistant type of tumor. Researchers believe that RIP1, which is found in most gliobrastomas, can be a therapeutic target for the highly blignant brain tumors.
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