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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.

  

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