a1 Department of Biology, Georgia State University, Atlanta, GA 30303, USA
a2 West Georgia Hospitals, LaGrange, GA 30240, USA
It is appreciated far and wide that increased and regular consumption of fruits and vegetables is linked with noteworthy anticancer benefits. Extensively consumed as a spice in foods and beverages worldwide, ginger (Zingiber officinale Roscoe) is an excellent source of several bioactive phenolics, including non-volatile pungent compounds such as gingerols, paradols, shogaols and gingerones. Ginger has been known to display anti-inflammatory, antioxidant and antiproliferative activities, indicating its promising role as a chemopreventive agent. Here, we show that whole ginger extract (GE) exerts significant growth-inhibitory and death-inductory effects in a spectrum of prostate cancer cells. Comprehensive studies have confirmed that GE perturbed cell-cycle progression, impaired reproductive capacity, modulated cell-cycle and apoptosis regulatory molecules and induced a caspase-driven, mitochondrially mediated apoptosis in human prostate cancer cells. Remarkably, daily oral feeding of 100 mg/kg body weight of GE inhibited growth and progression of PC-3 xenografts by approximately 56 % in nude mice, as shown by measurements of tumour volume. Tumour tissue from GE-treated mice showed reduced proliferation index and widespread apoptosis compared with controls, as determined by immunoblotting and immunohistochemical methods. Most importantly, GE did not exert any detectable toxicity in normal, rapidly dividing tissues such as gut and bone marrow. To the best of our knowledge, this is the first report to demonstrate the in vitro and in vivo anticancer activity of whole GE for the management of prostate cancer.
(Received February 03 2011)
(Revised April 04 2011)
(Accepted May 11 2011)
(Online publication August 18 2011)
Abbreviations: GE, ginger extract; HDF, human dermal primary fibroblast; IACUC, Institutional Animal Care and Use Committee; IC50, half-maximal concentration of growth inhibition; NCI, National Cancer Institute; PARP, poly(ADP-ribose)polymerase; PrEC, prostate epithelial cell; RPMI-1640, Roswell Park Memorial Institute-1640; TUNEL, terminal deoxynucleotidyl transferase dUTP nick-end labelling