Reversine suppresses oral squamous cell carcinoma via cell cycle arrest and concomitantly apoptosis and autophagy

<p>Abstract</p> <p>Background</p> <p>The effective therapies for oral cancer patients of stage III and IV are generally surgical excision and radiation combined with adjuvant chemotherapy using 5-Fu and Cisplatin. However, the five-year survival rate is still less than...

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Bibliographic Details
Main Authors: Lee Ying-Ray, Wu Wei-Ching, Ji Wen-Tsai, Chen Jeff, Cheng Ya-Ping, Chiang Ming-Ko, Chen Hau-Ren
Format: Article
Language:English
Published: BMC 2012-01-01
Series:Journal of Biomedical Science
Subjects:
Online Access:http://www.jbiomedsci.com/content/19/1/9
Description
Summary:<p>Abstract</p> <p>Background</p> <p>The effective therapies for oral cancer patients of stage III and IV are generally surgical excision and radiation combined with adjuvant chemotherapy using 5-Fu and Cisplatin. However, the five-year survival rate is still less than 30% in Taiwan. Therefore, evaluation of effective drugs for oral cancer treatment is an important issue. Many studies indicated that aurora kinases (A, B and C) were potential targets for cancer therapies. Reversine was proved to be a novel aurora kinases inhibitor with lower toxicity recently. In this study, the potentiality for reversine as an anticancer agent in oral squamous cell carcinoma (OSCC) was evaluated.</p> <p>Methods</p> <p>Effects of reversine on cell growth, cell cycle progress, apoptosis, and autophagy were evaluated mainly by cell counting, flow cytometry, immunoblot, and immunofluorescence.</p> <p>Results</p> <p>The results demonstrated that reversine significantly suppressed the proliferation of two OSCC cell lines (OC2 and OCSL) and markedly rendered cell cycle arrest at G2/M stage. Reversine also induced cell death via both caspase-dependent and -independent apoptosis. In addition, reversine could inhibit Akt/mTORC1 signaling pathway, accounting for its ability to induce autophagy.</p> <p>Conclusions</p> <p>Taken together, reversine suppresses growth of OSCC via multiple mechanisms, which may be a unique advantage for developing novel therapeutic regimens for treatment of oral cancer in the future.</p>
ISSN:1021-7770
1423-0127