Researchers at the University of Leeds found the E7 protein is produced early in the life cycle of the human papillomavirus (HPV) and blocks the body's natural defences against the uncontrolled division of cells that can lead to cancer.
Researchers have also synthesised a molecule, called an RNA aptamer, that latches onto the carcinogenic protein and targets it for destruction, significantly reducing its presence in cells in the laboratory derived from cervical cancers.
There are many types of human papillomavirus. Some are transmitted by sexual contact and associated not only with cervical cancer but also head and neck cancer.
"If we can use this aptamer to target the carcinogenic protein, we might be talking about much less radical surgery in the future," Stonehouse said.
Aptamers are a relatively new tool for molecular biologists and a topic of intense research interest. Like the much better understood antibodies, aptamers can identify and target other molecules as well as viruses and bacteria.
However, unlike traditional antibodies, they offer the possibility of insertion into live cells and can be artificially designed in the test tube.
"We were not trying to develop a therapy. We wanted to create better ways of looking at the virus infection because the current tools that we have are very limited," Stonehouse said.
"But what we found was that the aptamers caused the E7 protein to actually disappear. They seem to target it to be degraded. In a cell which is producing lots of E7 and is therefore dangerous, the level of E7 goes down if these RNA aptamers are there," Stonehouse added.
The new aptamer might be used in the future to help stop residual cancerous material from re-establishing itself after surgery and therefore allow less aggressive approaches to surgery.
The study was published in the journal PLOS One.
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