Although long-term survival in neurons means proper brain function as people get older, long-term
survival in brain cancer cells means tumor growth and spreading. According to a study published in
Science Signaling, the protein PARC/CUL9 promotes long-term survival in neurons and brain cancer
cells by overriding the biochemical mechanisms that lead to apoptosis, also known as cell death, in
This discovery indicates that brain cancer cells hijack the same mechanism that neurons
do in order to prolong their survival, which opens up further research for brain cancer treatments and
Parkinson’s disease, a prevalent neurodegenerative disease.
Senior author Mohanish Deshmukh and
researchers at University of North Carolina School of Medicine found that PARC and Parkin, a mutated
protein in Parkinson’s disease, are very similar. Researchers conducted experiments in cell cultures
and animal models. They damaged mitochondria, which usually releases cytochrome c, a protein that
activates the biochemical mechanism leading to cell death. However, researchers found that PARC/CUL9
impeded apoptosis by degrading cytochrome c.
Since researchers wanted to further study this process
in Parkinson’s disease, they used mouse models, but the mice did not share most of the hallmark
symptoms that human patients with Parkinson’s disease has.
They will continue their research on
Parkinson’s disease with new models and will study PARC as a target for cancer treatment as well.
Researchers at the UNC School of Medicine have discovered that the protein PARC/CUL9 helps neurons and brain cancer cells override the biochemical mechanisms that lead to cell death in most other cells. Vivian Gama, PhD, a postdoctoral fellow in Deshmukh’s lab, led the experiments in cell cultures and animal models.