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Oridonin induces G2/M cell cycle arrest and apoptosis in human oral squamous cell carcinoma
Han Wang1, Liping Zhu1, Xiaodong Feng1
1Department of Clinical Immunology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 639 Zhizaoju Road, Shanghai 200011, PR China.
Abstract:
Oridonin, an active diterpeniod isolated from Rabdosia rubescens, has been reported for its anti-tumor activity on several cancers, however, its effect on oral squamous cell carcinoma (OSCC) remains unclear. In this study, we demonstrated for the first time that oridonin inhibited the growth of OSCC cells both in vitro and in vivo. Oridonin decreased the proliferation and clonal formation of cultured OSCC cells in a dose-dependent manner. Further study indicated that oridonin induced G2/M phase arrest in OSCC cells, which was associated with the downregulation of proteins related to G2/M transition including cdc25C, cdc2 and cyclin B1, as well as the upregulation of p53 and phosphorylated-cdc2. In addition, we discovered that oridonin induced OSCC cell apoptosis by activating the intrinsic apoptotic pathway, which was indicated by the increased expression of cleaved-caspase 3, cleaved-caspase 9 and proapoptotic protein Bax and reduced expression of caspase 9 and antiapoptotic protein Bcl-xl. Finally, oridonin suppressed the growth of OSCC in an xenograft mouse model. Immunohistochemical analysis showed a reduction of cyclin B1-positive cancer cells and an increase of TUNEL-positive cancer cells in oridonin-treated mice. Therefore, oridonin may be a potentially effective agent for the treatment of OSCC in future.
Insights
Oridonin effectively inhibits oral squamous cell carcinoma (OSCC) growth by halting cell cycle progression and inducing apoptosis. This natural compound shows promise as a potential therapeutic agent for OSCC treatment.
Area of Science:
- Pharmacology
- Oncology
- Cell Biology
Background:
- Oridonin, a diterpenoid from Rabdosia rubescens, exhibits anti-tumor properties against various cancers.
- The therapeutic potential of oridonin in oral squamous cell carcinoma (OSCC) is not well-established.
Purpose of the Study:
- To investigate the anti-cancer effects of oridonin on oral squamous cell carcinoma (OSCC) cells.
- To elucidate the underlying mechanisms of oridonin-induced growth inhibition and apoptosis in OSCC.
Main Methods:
- In vitro studies assessed OSCC cell proliferation, clonal formation, and cell cycle distribution.
- Western blot analysis examined key proteins involved in cell cycle regulation and apoptosis.
- In vivo efficacy was evaluated using an OSCC xenograft mouse model with immunohistochemical analysis.
Main Results:
- Oridonin significantly inhibited OSCC cell proliferation and colony formation in a dose-dependent manner.
- Oridonin induced G2/M phase arrest by modulating proteins like cdc25C, cdc2, cyclin B1, and p53.
- Oridonin triggered apoptosis via the intrinsic pathway, evidenced by altered expression of caspases and Bcl-2 family proteins.
- In vivo, oridonin suppressed tumor growth and reduced cyclin B1 expression while increasing apoptosis markers in xenograft models.
Conclusions:
- Oridonin demonstrates significant anti-cancer activity against oral squamous cell carcinoma (OSCC) both in vitro and in vivo.
- Oridonin exerts its effects by inducing cell cycle arrest and apoptosis.
- Oridonin represents a promising candidate for future development as an OSCC therapeutic agent.
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