Allitridi induces apoptosis by affecting Bcl-2 expression and caspase-3 activity in human gastric cancer cells.
OBJECTIVE
To investigate the mechanism of allitridi-induced apoptosis in human gastric cancer cell line BGC823.


METHODS
Growth inhibition by allitridi was analyzed using cell growth curve and MTT assay. Apoptotic cells were detected using staining with Hoechst 33342, and confirmed by flow cytometric analysis and DNA fragmentation analysis. The protein expression affected by allitridi was determined using Western blot. The activity of caspase-3 was measured using a fluorescence assay.


RESULTS
Allitridi induced apoptosis, and then inhibited cells proliferation in human gastric cancer cell line BGC823. The protein level of Bcl-2 was decreased dramatically, while Bax and p53 were not significantly affected by allitridi. The expression and activity of caspase-3 started to increase after allitridi treatment for 72 h.


CONCLUSIONS
Allitridi induced apoptosis through down-regulation of Bcl-2, and increased caspase-3 expression and its activity.
Lan
Hong
H
Beijing Molecular Oncology, Beijing Institute for Cancer Research, School of Oncology, Peking University, Beijing 100034, China.
Lü
You-yong
YY
D000230:Adenocarcinoma / Q000378:metabolism / Q000473:pathology; D000498:Allyl Compounds / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D053148:Caspase 3; D020169:Caspases / Q000378:metabolism*; D045744:Cell Line, Tumor; D015536:Down-Regulation; D006801:Humans; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis*; D013274:Stomach Neoplasms / Q000378:metabolism / Q000473:pathology*; D013440:Sulfides / Q000494:pharmacology*
D000498:Allyl Compounds; D019253:Proto-Oncogene Proteins c-bcl-2; D013440:Sulfides; C042577:diallyl trisulfide; C505407:CASP3 protein, human; D053148:Caspase 3; D020169:Caspases