Researchers have identified a tumor-suppressing protein in the brains of fruit flies, called PP2A (protein phosphatase 2A), which has a counterpart in mammals.
This work attains significance because it holds promise to prevent the formation of brain tumors in humans, say the researchers at Duke-NUS Graduate Medical School in Singapore.
"Our data explicitly show that the fruit-fly protein PP2A (protein phosphatase 2A) suppresses brain tumor formation and controls the balance of self-renewal and differentiation of neural stem cells," said Dr. Hongyan Wang, senior author of the study.
"Given that mechanisms for stem cell division in flies and mammals are likely to be similar, our study on fly PP2A may provide useful insights for certain types of human brain tumors and possibly in a wide variety of cancers," said Wang.
The researchers studied flies that had a PP2A mutation and learned that the flies with missing or abnormally expressed PP2A had ten times the amount of stem cell growth in their larval brains.
The flies' neural stem cells did not become neurons (nerve cells) in the brain, the types of cells needed for normal function. But they effectively grew into a tumor mass.
In an earlier study, the researchers had identified a protein kinase called Polo as a tumor suppressor.
As phosphatases like PP2A usually have the opposite biochemical function to kinase, the scientists predicted that PP2A would stop the tumor suppressor Polo and allow for unchecked cell growth.
"We were very surprised when we found that PP2A also suppressed tumors," said Wang.
Follow-up experiments showed that PP2A is important for regulating Polo kinase function, and showed that these two critical brain tumor suppressors work in tandem to control neural stem cell divisions.
"Our discovery suggests that PP2A and Polo, both of which are crucial brain tumor-suppressors and cell cycle regulators, can function in the same pathway to regulate stem cell self-renewal and tumor development," said Wang.
The study has been published online in the journal Development.