Traditional Herbal Medicine Kills Pancreatic Cancer Cells, Jefferson Researchers Report
An
herb used in traditional medicine by many Middle Eastern countries may
help in the fight against pancreatic cancer, one of the most difficult
cancers to treat. Researchers at the Kimmel Cancer at Jefferson in
Philadelphia have found that thymoquinone, an extract of nigella sativa
seed oil, blocked pancreatic cancer cell growth and killed the cells by
enhancing the process of programmed cell death.
While
the studies are in the early stages, the findings suggest that
thymoquinone could eventually have some use as a preventative strategy
in patients who have gone through surgery and chemotherapy or in
individuals who are at a high risk of developing cancer.
According
to Hwyda Arafat, M.D., Ph.D., associate professor of Surgery at
Jefferson Medical College of Thomas Jefferson University, nigella
sativa helps treat a broad array of diseases, including some immune and
inflammatory disorders. Previous studies also have shown anticancer
activity in prostate and colon cancers, as well as antioxidant and
anti-inflammatory effects.
Using
a human pancreatic cancer cell line, she and her team found that adding
thymoquinone killed approximately 80 percent of the cancer cells. They
demonstrated that thymoquinone triggered programmed cell death in the
cells, and that a number of important genes, including p53, Bax, bcl-2
and p21, were affected. The researchers found that expression of p53, a
tumor suppressor gene, and Bax, a gene that promotes programmed cell
death, was increased, while bcl-2, which blocks such cell death, was
decreased. The p21 gene, which is involved in the regulation of
different phases of the cell cycle, was substantially increased. She
presents her findings May 18 at the Digestive Disease Week in San
Diego.
Dr.
Arafat and her co-workers also found that thymoquinone caused
“epigenetic” changes in pancreatic cancer cells, modifying the cells’
DNA. She explains that these changes involve adding acetyl groups to
the DNA structure, specifically to blocks of proteins called histones.
This “acetylation” process can be important for genes to be read and
translated into proteins. In this case, it could involve the genes that
are key to initiating programmed cell death.
“We looked at the status of the histones and found surprisingly that thymoquinone increased the acetylation process,” Dr.
Arafat says. “We never anticipated that.”
At
the same time, adding thymoquinone to pancreatic cancer cells reduced
the production and activity of enzymes called histone deacetylases
(HDACs), which remove the acetyl groups from the histone proteins,
halting the gene transcription process. Dr. Arafat notes that HDAC
inhibitors are a “hot” new class of drugs that interfere with the
function of histone deacetylases, and is being studied as a treatment
for cancer and neurodegenerative diseases. Finding that thymoquinone
functions as an HDAC inhibitor, she says, “was very remarkable and
really exciting.”
Pancreatic
cancer, the fourth-leading cause of cancer death in this country, takes
some 34,000 lives a year. The disease frequently is detected after it
has spread and only 4 percent of individuals with pancreatic cancer
live for five years after diagnosis.
Media Only Contact:
Steve Benowitz
Thomas Jefferson University Hospital
Phone: (215) 955-6300
Published: 5/19/2008