New research from Georgetown University in Washington, D.C., investigates how the human papillomavirus promotes cancer. The findings might point to a potential new and improved strategy for targeted treatment.
According to data from the Centres for Disease Control and Prevention (CDC), around 1 in 4 people in the United States are infected with HPV.
Although treatments for HPV-related conditions do exist, they either target non-cancerous outcomes (such as genital warts) or they focus on the prevention of cancer through screening of abnormal cell activity.
Treatments for cancers caused by HPV include surgical interventions and chemotherapy, but at present, none of the options specifically address the viral source.
Researchers from Georgetown University Medical Center in Washington, D.C., have now identified the mechanism that promotes the survival of cancerous cells due to HPV.
The study, which was led by Dr. Xuefeng Liu, describes a molecular apparatus that renders cancer cells “immortal.” Understanding how this apparatus works may lead to better targeted treatments in the future, the researcher suggests.
“There is no targeted treatment now for these cancers since German virologist Harald zur Hausen, Ph.D., discovered in 1983 that HPV can cause cervical cancer,” says Dr. Liu.
“Recently,” he adds, “the numbers of HPV-linked head and neck cancers have increased in the U.S. Now we have a chance to develop and test a very specific, potentially less toxic way to stop these cancers.”
The researchers’ findings are published in the journal Oncotarget.
Previous research conducted by Dr. Liu and his team uncovered the role of an HPV oncoprotein – a protein encoded by an oncogene, or gene that may cause cancer – called E6, in supporting cancer tumors.
The researchers noted that HPV E6 interferes with a tumor suppressor protein called p53, increasing telomerase activity in cancer cells.
Telomerase is an enzyme that plays a role in cell survival and death. In normal cells, telomerase is usually not active, meaning that those cells eventually die.
In cancer cells, telomerase is present in high quantities. When it is “switched on” and becomes active, it prolongs the life of these infected cells, meaning that they cannot die naturally.
By interfering with p53, HPV E6 boosts telomerase activity in cancer cells, prolonging their survival rate and thus supporting tumor growth.
In the study, Dr. Liu and colleagues uncovered another key interaction. HPV E6, they noted, also influences a protein called myc – encoded by the Myc gene – which plays a role in cell death, or apoptosis, and in the regulation of cell division.
The researchers found that telomerase activity in cancer cells is boosted when E6 molecules bond with myc molecules.
What this suggests is that, by designing a molecule that could interfere with E6-myc interaction, researchers might be able to prevent the increased telomere activity in cancer cells, thus making them more likely to undergo cell death.
Dr. Liu explains that the new molecule might bind to E6 instead of myc, or vice versa, thus blocking any interaction between the two.
“This small molecule would not be toxic to all normal cells or, importantly, to master stem cells, because myc would not be affected. It could be a unique treatment, targeted specifically to HPV cancers.”
Dr. Xuefeng Liu
Currently, Dr. Liu and other researchers from Georgetown University are already experimenting with a way of interfering with the mechanism that allows HPV to support cancerous tumor growth.