|
THE PHARMA REVIEW
(NOVEMBER 2009) |
Therapeutic Potential of
Curcumin in Prostate Cancer
|
|
R.A. Hajare, S.A. Bajad, K.S.
Parwani, N.A.Chandekar, A.V.Chandewar |
|
Abstract: Prostate cancer is the second leading
cause of cancer death in men. There is increasing
evidence that the stringent selective pressure imposed
by androgen ablation therapy on the residual prostate
cancer cells may actually accelerate the development of
the hormone refractory and bone metastatic phenotype.
The propensity of prostate cancer to establish osseous
metastases is very likely mediated by the osteomimetic
properties of the prostate cancer cells. Prostate cancer
cells acquire these “bone-like” properties in order to
survive in the bony microenvironment. This process is
facilitated by common growth factor trophisms between
the bone stromal cells, osteoblasts, and the prostate
cancer cells wherein a number of growth factors and
their receptors are involved. Thus, a general inhibition
of the tyrosine kinase signaling pathways may have a
therapeutic advantage in interfering with the metastatic
potential of these prostate cancer cells. This study
focuses on the potential of curcumin, a plant based
non-toxic tyrosine kinase inhibitor in interfering with
the development of bone like properties of C4-2B, a
highly metastatic derivative of LNCaP prostate cancer
cell line.
Introduction
Curcumin (Diferuoylmethane), the yellow pigment in the
rhizome of turmeric (Curcuma longa), an ingredient of
curry spice, is known to exhibit a variety of
pharmacological effects including antitumor,
anti-inflammatory, and antiinfectious activities.
Although its precise mode of action remains elusive,
curcumin has been shown to suppress the activity of the
AP-1 transcription factor in cells stimulated to
proliferate. In this study, we predict that curcumin
inhibited proliferation of thymocytes stimulated with
concanavalin A (Con A) as well as that of human Jurkat
lymphoblastoid cells in the logarithmic growth phase.
The induction of apoptosis by curcumin in thymocytes was
accompanied by partial suppression of AP-1 activity.
Complete suppression of AP-1 activity was observed in
Con A-treated, proliferating thymocytes. The capacity of
curcumin to inhibit both cell growth and death strongly
implies that these two biological processes share a
common pathway at some point and that curcumin affects a
common step, presumably involving a modulation of the
AP-1 transcription factor.
For full text of this article contact the publisher on
info@kppub.com
|
|
Go to Content Index Page
|
|
The above content is an
abstract only. For the full Article please contact:
KONGPOSH Publications Pvt. Ltd.
ICS House, C-19, Commercial Complex, SDA, Opp. IIT Gate,
New Delhi, India -110016
Tel.: 26855839, 20057149, Fax: 91-11-26855876
Email:
info@kppub.com /
fpc@vsnl.com, Website:
http://www.kppub.com |
|
|
|
