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Published on: December 1, 2013
Thymol inhibits bladder cancer cell proliferation via inducing cell cycle arrest and apoptosis
Yi Li1, Jia-Ming Wen2, Chuan-Jun Du2
1Department of Urology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China; Department of Surgical Oncology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China; Cancer Institute, Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education, Key Laboratory of Molecular Biology in Medical Sciences, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China; Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY, USA.
Abstract:
Thymol is a phenolic compound with various pharmacological activities such as anti-inflammatory, anti-bacterial and anti-tumor effects. However, the effect of thymol on bladder cancer cell growth is still elusive. The purpose of this study is to investigate the efficacy of thymol in bladder cancer cells and its underlying mechanism. Thymol inhibited bladder cancer cell proliferation in a dose and time-dependent manner. We also observed cell cycle arrest at the G2/M phase after the treatment of thymol. Moreover, thymol could induce apoptosis in bladder cancer cells via the intrinsic pathway along with caspase-3/9 activation, release of cytochrome c and down-regulation of anti-apoptotic Bcl-2 family proteins. The activation of JNK and p38 was also critical for thymol-induced apoptosis since it was abrogated by the treatment of JNK inhibitor (SP600125), and p38 inhibitor (SB203580) but not ERK inhibitor (SCH772984). Furthermore, the generation of ROS (reactive oxygen species) was detected after the treatment of thymol. ROS scavenger NAC (N-acetyl cysteine) could block the thymol-triggered apoptosis and activation of MAPKs. These findings offer a novel therapeutic approach for bladder cancer.
Insights
Thymol effectively inhibits bladder cancer cell growth by inducing cell cycle arrest and apoptosis. This natural compound triggers programmed cell death through the intrinsic pathway, involving reactive oxygen species and MAPK signaling.
Area of Science:
- Oncology
- Pharmacology
- Cell Biology
Background:
- Thymol, a natural phenolic compound, exhibits diverse pharmacological properties including anti-inflammatory, anti-bacterial, and anti-tumor effects.
- The specific impact of thymol on bladder cancer cell proliferation and its underlying molecular mechanisms remain largely unexplored.
Purpose of the Study:
- To investigate the anti-cancer efficacy of thymol in bladder cancer cells.
- To elucidate the molecular pathways mediating thymol's effects on bladder cancer.
Main Methods:
- Bladder cancer cell lines were treated with varying concentrations of thymol.
- Cell proliferation, cell cycle progression, apoptosis, and key signaling pathways (MAPKs, Bcl-2 family, caspases) were analyzed.
- Reactive oxygen species (ROS) generation was assessed, and the role of ROS was evaluated using a scavenger.
Main Results:
- Thymol significantly inhibited bladder cancer cell proliferation in a dose- and time-dependent manner.
- Thymol induced cell cycle arrest at the G2/M phase and triggered apoptosis via the intrinsic pathway, evidenced by caspase activation, cytochrome c release, and Bcl-2 family protein modulation.
- Thymol-induced apoptosis was dependent on JNK and p38 MAPK activation and involved ROS generation, as confirmed by inhibitor studies and ROS scavenger treatment.
Conclusions:
- Thymol demonstrates potent anti-proliferative and pro-apoptotic effects on bladder cancer cells.
- The mechanism involves ROS generation, MAPK signaling (JNK/p38), and induction of the intrinsic apoptotic pathway.
- Thymol represents a promising therapeutic candidate for bladder cancer treatment.
