Researchers at London’s Institute of Cancer Research have found that mutations in a Parkinson’s disease gene called PARK2 can be found in a third of all human cancers and play a role in helping cancer cells survive.
The study “PARK2 Depletion Connects Energy and Oxidative Stress to PI3K/Akt Activation via PTEN S-Nitrosylation” appeared in the journal Molecular Cell.
According to researchers, PARK2 gene mutations have been found in as high as 77 percent of Parkinson’s disease cases with an onset age of less than 20 years, and in 3 percent of patients with an age of onset of more than 30 years.
This gene encodes a protein that helps the mitochondria produce energy, so when mutations occur, these components stop functioning normally. In the brain, this typically leads to neuronal death, but in cancer cells, other mechanisms compensate for the loss of PARK2 and normal mitochondrial activity to help them survive.
Researchers analyzed 10,000 tumor samples from 28 types of cancer, and found mutations of the PARK2 gene in more than a third of cancer types.
Further experiments showed that mutations causing the loss of PARK2 in cancer cells activated a survival mechanism called the PI3K/Akt pathway and inhibited the PTEN gene, which is known to suppress tumor activity. Indeed, PARK2 levels fell significantly in many cancer types, meaning a poor prognosis for patients with brain, breast and lung cancer.
“Our study has highlighted that PARK2 loss is present in around a third of all cancers and has profound implications in understanding how cancer cells may support their proliferation and survival under conditions of [energy] deprivation,” the study’s senior author, George Poulogiannis, said in a news release.
The study also links PARK2 with cancer development. This information may help find novel treatments against PARK2 mutations.
“In the future, tests that look for mutations to PARK2 may help to identify patients who have particularly aggressive forms of cancer that may respond to inhibitors of PI3K/Akt signaling,” Poulogiannis concluded.
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