The aim of this study was to investigate the effect of
Paris saponin I (PS I) on human gastric
carcinoma cell growth and apoptosis and to explore the potential mechanisms. The proliferation of SGC7901 cells was monitored by the MTT cell viability assay, while the nuclear morphology of apoptotic cells was assessed by
Hoechst 33258 staining. Flow cytometry was performed to analyze the cell cycle progression of
propidium iodide (PI)-stained SGC7901 cells and the apoptotic rate of
annexin V/PI-stained cells. Western blotting was used to examine the expression of several
cell cycle proteins, including
cyclin B1 and Cdk1, and the apoptosis-regulated
proteins Bcl-2, Bax,
cytochrome c,
procaspase-9, and
procaspase-3. The MTT assay demonstrated that PS I could induce significant dose- and time-dependent inhibition of SGC7901 cell proliferation. Marked morphological changes, including condensation of
chromatin, nuclear fragmentation and apoptotic bodies were clearly shown on
Hoechst 33258 staining. PSI treatment also resulted in the disruption of the cell cycle at G₂/M and the induction of apoptosis. Following PSI treatment, the cell cycle-related
proteins cyclin B1 and Cdk1 were down-regulated. Expression of the
pro-apoptotic protein Bax was increased, while
anti-apoptotic protein Bcl-2 decreased. PSI treatment resulted in elevated cytoplasmic
cytochrome c and activation of the apoptotic
proteases caspase-9 and
caspase-3. These data indicate that PS acts as an inhibitor of proli I feration in SGC7901 cells by inducing cell cycle arrest and mitochondria-dependent apoptosis. PSI is a potential therapeutic agent against human gastric
carcinoma.