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

Ho,Jin‑Nyoung; Kang,Minyong; Lee,Sangchul; Oh,Jong Jin; Hong,Sung Kyu; Lee,Sang Eun; Byun,Seok‑Soo

doi:10.3892/ol.2017.7280

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

Authors:
- Jin‑Nyoung Ho
- Minyong Kang
- Sangchul Lee
- Jong Jin Oh
- Sung Kyu Hong
- Sang Eun Lee
- Seok‑Soo Byun
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Affiliations: Department of Urology, Seoul National University College of Medicine, Seoul National University Bundang Hospital, Seongnam‑si, Gyunggi‑do 463‑707, Republic of Korea, Department of Urology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul 135‑710, Republic of Korea
Published online on: October 26, 2017 https://doi.org/10.3892/ol.2017.7280
Pages: 623-629

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Abstract

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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