Scientists identify waste disposal protein that is key to cancer tumour suppression

Washington, June 12 (ANI): American scientists have identified a waste disposal protein, which is key to cancer tumour suppression in a process known as autophagy, in which cancer cells eat themselves.

The finding attains significance because it may for the first time help scientists' understand the mechanism that makes autophagy a pathway to cancer tumour suppression.

Researchers at The Cancer Institute of New Jersey (CINJ) and Rutgers, The State University of New Jersey, have revealed that their research focuses on a protein known as p62.

Writing about their work in the journal Cell, the researchers reveal that this protein is responsible for disposing of damaged proteins that accumulate in a cell, when it is no longer receiving nourishment for growth and is under other environmental stress.

The researchers write that in cells need to rid themselves of this waste to prevent themselves from becoming a cancer tumour.

According to them, the p62 protein packages the damaged materials and prepares them, along with itself, to be degraded through the autophagy process.

The researchers say that disruption in the process or failure to dispose of p62 from the cell can result in toxicity, genome damage and inflammation, which in turn can promote tumour progression.

Senior author Dr. Eileen White, associate director for basic science at CINJ, notes that this is the first time the disposal of p62 has been linked with tumour suppression, which can be key in cancer prevention.

"This discovery is important, because we now have an opportunity to look at people at risk for cancer before it develops. These latest findings show that p62 can act as a marker to identify certain cancers and that we can manipulate p62 levels to stimulate the process of autophagy and ultimately tumour suppression," she notes

For their study, the researchers looked at both mouse models and human tissue samples from liver, lung and kidney tumours.

White indicates that there is evidence that controlling p62 levels also has implications in lymphoma and breast and prostate cancers.

Considering that diseases like Alzheimer's, Parkinson's and Huntington's share the same property of failing to dispose of protein waste properly, White says that the latest discovery involving the p62 protein also has implications for further unlocking the mysteries of neurodegenerative disorders and for providing tools for new drug discovery.

She notes tjat further understanding of the p62 mechanism in relation to this functional consequence is necessary, as induction of autophagy during treatment can be counterproductive.

She says that future studies should include trying to identify new or existing drugs that will enhance the autophagy process so that novel mechanisms for tumour prevention can be established. (ANI)