By manipulating HuR, researchers are able to kill drug resistant pancreatic cancer cells.
A recent study found that a protein called Hu antigern R (HuR) is a center for cancer cell survival and drug resistance, especially in pancreatic cancer cells previously treated with Tumor necrosis factor-Related Apoptosis Inducing Ligand (TRAIL).
In previous studies, researchers worked on cancer therapy by mimicking TRAIL, a naturally occurring compound that triggers cells to self-destruct.
In humans, TRAIL-mimicking drugs were not effective typically because the cancer cells quickly became resistant.
In the current study, researchers found that cancer cells treated with TRAIL activate HuR. Once activated, the amount of death receptors are reduced, making TRAIL-mimicking drugs less effective.
Using short interfering RNA or a small molecule chemical blocker, researchers were able to block HuR and TRAIL-mimicking drugs were found to work better.
According to the study, in some trials, twice as many pancreatic cancer cells died from TRAIL-drug treatment.
"Although these results will not change treatment options for patients today, they give us a glimmer of hope that we can salvage therapies that have already advanced to human clinical trials and are therefore closer to human use than novel therapies," said study author Carmella Romeo.
Researchers predict that blocking HuR could lead to the revival of cancer drugs that trigger self-destructing mechanisms in cancer cells.