SUPPRESSING a specific protein could be an effective way of combatting pancreatic cancer, according to a new study performed by researchers from the Keck School of Medicine, University of Southern California, Los Angeles, California, USA. This is the first study to show that the protein, GRP78, plays a vital role in ‘switching’ healthy pancreatic cells into potentially cancerous cells.
GRP78 is a glucose-regulated protein that is sent to the cell surface during stress to assist in growth and survival. Cancer cells, particularly those which survive treatment, generally undergo more stress than healthy cells and are therefore exposed to an abundance of GRP78, which aids their survival, increases their ability to thrive, and helps develop therapeutic resistance. “Cancer cells are addicted to high levels of GRP78 for cancer development and growth. Our hope is that partially reducing or inactivating the protein by therapeutic agents could one day be an effective complementary therapy for pancreatic cancer and other cancers, while sparing other healthy organs,” explained Prof Amy Lee, Keck School of Medicine.
Studies on GRP78 suppression were conducted in mice with the KRAS genetic mutation, present in 90% of pancreatic cancer patients. Results were promising, showing that expressing just half the amount of GRP78 was enough to halt the earliest stages of pancreatic cancer development.
Prof Lee commented: “As developing drugs directly targeting the KRAS genetic mutation has been challenging, we are thrilled these findings indicate that we can attack KRAS-driven pancreatic cancer through an entirely new method.” The development of potential treatments that can inhibit GRP78 activity and expression are underway, some of which are already showing positive results in early clinical trials.
Pancreatic cancer is predicted to be diagnosed in >53,600 people in the USA this year and is one of the deadliest forms of cancer, with a 5-year survival rate of just 12% in early stage patients. “Given the notorious difficulties of treating KRAS-mutation related cancers, particularly in a disease as devastating as pancreatic cancer, this research provides hope and a novel approach. I am excited to put our theories to test in the clinical setting,” concluded Prof Lee.
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