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Researchers identify novel approach for
suppressing Prostate Cancer development
Newswise — Researchers at the University of
Southern California (USC) have found that
inactivating a specific biomarker for
aggressive prostate cancer blocks the
development of prostate cancer in animal
models.
Researchers say the upcoming study in the
Proceedings of the National Academy of
Sciences—now available online—may lead to a
novel cancer therapy for humans.
“This research has far-reaching implications
in a wide range for human cancers,” says Amy
Lee, Ph.D., the study’s principal
investigator and the associate director for
basic research and holder of the Freeman
Cosmetics Chair at the USC/Norris
Comprehensive Cancer Center, and professor
of biochemistry and molecular biology at the
Keck School of Medicine of USC. "It is a
breakthrough study.”
Prostate cancer is the most common cancer in
men and develops through successive stages.
The glucose-regulated protein GRP78 has been
identified as a crucial entity in the
development of prostate cancer by promoting
cancer cell proliferation, mediating
oncogenic signaling and protecting cancer
cells against cell death resulting from the
stress of tumor development, Lee explains.
By suppressing GRP78 expression or activity,
the USC researchers found that they could
block prostate cancer activation and
development resulting from the loss of PTEN,
a powerful tumor suppressor gene for a
number of human cancers.
Researchers spent more than three years
monitoring prostate cancer development in
animal models that had been genetically
engineered to have both the GRP78 and PTEN
tumor suppressor genes inactivated.
The research was conducted by Yong Fu, a
Ph.D. candidate at the Keck School of
Medicine of USC and the first author on the
study, in collaboration with Ph.D candidates
Shiuan Wey, Miao Wang, Risheng Ye and Chun-Peng
Liao and Pradip Roy-Burman, M.D., professor
of pathology, biochemistry and molecular
biology at the Keck School.
Future research should test the role of
GRP78 in other types of cancer and isolate
drugs that inhibit GRP78, Lee says.
“To our knowledge, this is the first
demonstration that inactivation of a
specific molecular chaperone from the mouse
prostate epithelial cells can potently block
prostate cancer development and suppress the
activation of AKT, which is a protein kinase
that promotes cell proliferation and
survival and is a major factor in many types
of cancer,” Lee says.
“With the recent advances in identifying
agents that suppress GRP78 expression,
anti-GRP78 therapy may open up an entirely
new approach to stop human cancer.”
The study was funded by a grant from the
National Cancer Institute that has been
awarded to Amy Lee for the past 28 years.
Yong Fu, Shiuan Wey, Miao Wang, Risheng Ye,
Chun-Peng Liao, Pradip Roy-Burman, and Amy
S. Lee. "Pten null prostate tumorigenesis
and AKT activation are blocked by targeted
knockout of ER chaperone GRP78/BiP in
prostate epithelium." Proceedings of
National Academy of Sciences. Nov. 2008.
http://www.pnas.org/content/early/recent
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