Anticancer effect of S-allyl-L-cysteine via induction of apoptosis in human bladder cancer cells

被引:22
|
作者
Ho, Jin-Nyoung [1 ]
Kang, Minyong [2 ]
Lee, Sangchul [1 ]
Oh, Jong Jin [1 ]
Hong, Sung Kyu [1 ]
Lee, Sang Eun [1 ]
Byun, Seok-Soo [1 ]
机构
[1] Seoul Natl Univ, Coll Med, Dept Urol, Bundang Hosp, 166 Gumi Ro, Seongnam Si 463707, Gyunggi Do, South Korea
[2] Sungkyunkwan Univ, Dept Urol, Samsung Med Ctr, Sch Med, Seoul 135710, South Korea
关键词
bladder cancer cells; S-allyl-L-cysteine; anticancer; apoptosis; cell cycle; CYCLE ARREST; IN-VITRO; PROLIFERATION; ALLYLCYSTEINE; INHIBITION;
D O I
10.3892/ol.2017.7280
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
To examine the anticancer effects of S-allyl-L-cysteine (SAC) in human bladder cancer cells and to identify possible molecular mechanisms, bladder cancer cell lines (HTB5, HTB9, JON, UMUC14, T24, and cisplatin resistant-T24R2) were incubated with SAC, and cell proliferation was measured using the Cell Counting Kit-8 assay and clonogenic assay. Cell cycle and apoptosis were evaluated by flow cytometry. Expression levels of apoptosis- and cell cycle-associated proteins were analyzed by western blotting. Proliferation and colony formation in bladder cancer cells was significantly inhibited by SAC treatment in a dose-dependent manner. SAC treatment significantly enhanced apoptosis and promoted a cell cycle arrest in the S phase. SAC also increased the expression of apoptosis-related genes, including caspases, poly (ADP-ribose) polymerase and cytochrome c. SAC had an anticancer effect on bladder cancer cells in vitro, at least partially, through the induction of apoptosis and a cell cycle arrest. SAC is a potential therapeutic agent for the treatment of bladder cancer.
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页码:623 / 629
页数:7
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