A new way to disrupt the process of pancreatic cancer cells and slow down their mobility has been identified by researchers.
Often, and without much warning, pancreatic cancer cells slip through the endothelial cells, head into the blood and out to other parts of the body to metastasize, making it one of the deadliest and hardest to treat cancers today.
Now, researchers from Thomas Jefferson University's Center for Translational Medicine have found that reducing levels of a well known, cell-surface protein known as N-cadherin in those cancer cells can interfere with that activity.
They found that the disruption slowed down the pancreatic cancer cells' mobility, and prolonged survival in mice.
The findings support a critical role for N-cadherin in pancreatic ductal adenocarcinma (PDA). Because this cancer does not typically produce symptoms until after it has metastasized, the mortality rate is very high-its five-year survival rate is less than 5 percent.
Thus, strategies that specifically target and prevent the spreading of the cancer cells have the potential to significantly improve the prognosis for patients.
"Previous studies demonstrated the importance of this cell surface protein for tumour cell growth," said Glenn Radice, Ph.D., an Associate Professor in the Department of Medicine at Jefferson's Center for Translational Medicine, and co-author of the study.
"However, it was not clear from those studies whether interfering with N-cadherin levels would increase survival of animals genetically engineered to develop highly metastatic pancreatic cancer," he noted.
Using the mouse model, researchers found that reducing N-cadherin expression delayed tumour progression and prolonged survival in mice by 25 percent.
The finding has been published online in December in Nature's Oncogene.