RT Journal Article
SR Electronic
T1 Gypenosides Induced G0/G1 Arrest <em>via</em> Inhibition of Cyclin E and Induction of Apoptosis <em>via</em> Activation of Caspases-3 and -9 in Human Lung Cancer A-549 Cells
JF In Vivo
JO In Vivo
FD International Institute of Anticancer Research
SP 215
OP 221
VO 22
IS 2
A1 LU, HSU-FENG
A1 CHEN, YI-SHAN
A1 YANG, JAI-SING
A1 CHEN, JUNG-CHOU
A1 LU, KUNG-WEN
A1 CHIU, TSAN-HUNG
A1 LIU, KUO-CHING
A1 YEH, CHIN-CHUNG
A1 CHEN, GUANG-WEI
A1 LIN, HUI-JU
A1 CHUNG, JING-GUNG
YR 2008
UL http://iv.iiarjournals.org/content/22/2/215.abstract
AB Gynostemma pentaphyllum Makino is known in Asia for its effect on the treatment of hepatitis and cardiovascular diseases. Gypenosides (Gyp) are the major components extracted from Gynostemma pentaphyllum Makino. However, the molecular mechanism underlying the Gyp-induced cell cycle arrest and apoptotic process is unclear. In this study, the chemopreventive role of Gyp in human lung cancer (A549) cells in vitro was evaluated by studying the regulation of the cell cycle and apoptosis. Gyp induced G0/G1 arrest and apoptosis in the human lung cancer A549 cells. Investigation of the cyclin-dependent protein kinase inhibitors by Western blotting showed that p16, p21, p27 and p53 proteins were increased with the increasing time of incubation with Gyp in the A549 cells. This increase may be the major factor by which Gyp caused G0/G1 arrest in the examined cells. Flow cytometric assay and gel electrophoresis of DNA fragmentation also confirmed that Gyp induced apoptosis in the A549 cells. Our data demonstrated that Gyp-induced apoptotic cell death was accompanied by up-regulation of Bax, caspase-3 and caspase-9, but down-regulation of the Bcl-2 levels. Taken together, Gyp appears to exert its anticancer properties by inducing G0/G1-phase arrest and apoptosis via activation of caspase-3 in human lung A549 cancer cells. Copyright © 2008 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved