Researchers at The University of Texas Southwestern Medical Center found that the protein RIP1 acts as a mediator of brain tumour cell survival, either protecting or destroying cells.
Researchers believe that the protein, found in most glioblastomas, can be targeted to develop a drug treatment for these highly malignant brain tumours.
"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.
In the study, researchers used animal models to examine the interactions of the cell receptor EGFRvIII and RIP1. Both are used to activate NF-kappaB, a family of proteins that is important to the growth of cancerous tumour cells.
When RIP1 is switched off in the experimental model, NF-kappaB and the signalling that promotes tumour growth is also inhibited.
Furthermore, the findings show that RIP1 can be activated to divert cancer cells into a death mode so that they self-destruct.
The study was published in journal Cell Reports.
