CHINESE HERBAL EXTRACT MAY KILL PANCREATIC CANCER CELLS
A diagnosis of pancreatic cancer—the fourth
most common cause of cancer death in the U.S.—can be devastating. Due in part to
aggressive cell replication and tumor growth, pancreatic cancer progresses
quickly and has a low five-year survival rate (less than 5 percent).
GRP78,
a protein that protects cells from dying, is more abundant in cancer cells and
tissue than in normal organs and is thought to play a role in helping
pancreatic cancer cells survive and thrive. Researchers at the University of
Minnesota have found triptolide, an extract of the Chinese herb thunder god
vine (Tirpterygium wilforii), suppresses GRP78, eventually leading to
pancreatic cancer cell death.
For
mammals to use the proteins in our bodies, a process called protein folding
must occur in the endoplasmic reticulum (ER) of cells. If proteins are not
folded fast enough, unfolded proteins begin to build up and the cell becomes
stressed. Prolonged ER stress activates a cellular process called the “unfolded
protein response (UPR)”. Initially, the UPR helps kick-start the cell’s
protein-folding ability, allowing it to function properly again. But if the
problem doesn’t resolve, the UPR triggers cell death.
GRP78
helps cells survive long enough for the UPR to kick in and correct
protein-folding problems. However, GRP78 is available in higher quantities in
pancreatic cancer cells, which assists the cancer cells in evading cell death,
allowing them to live and multiply.
Triptolide has previously been shown to have a negative effect on pancreatic
cancer cell viability and to block growth and spread of these cells. In this
study led by Ashok Saluja, Ph.D., researchers observed the effects of
triptolide on human pancreatic cancer cells and tissue. They found that the UPR
worked properly in triptolide-treated cells to allow cell death in
malfunctioning cells.
Our study shows that although
increased expression of GRP78 confers a survival advantage to the tumor cells,
prolonged exposure to triptolide induces chronic ER stress, which eventually
leads to cell death,” the authors stated. “In this context, inhibition of GRP78
by activation of the ER stress pathway by triptolide offers a novel mechanism
for inhibiting the growth and survival of pancreatic cancer cells.”
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