Effects of roniciclib in preclinical models of anaplastic thyroid cancer
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Shu-Fu Lin1, Jen-Der Lin1, Chuen Hsueh2, Ting-Chao Chou3,4 and Richard J. Wong5
1Department of Internal Medicine, Chang Gung Memorial Hospital, Chang Gung University, Taoyuan, Taiwan
2Department of Pathology, Chang Gung Memorial Hospital, Chang Gung University, Taoyuan, Taiwan
3Laboratory of Preclinical Pharmacology Core, Memorial Sloan Kettering Cancer Center, New York, NY, USA
4Current address: PD Science, Inc., Paramus, NJ, USA
5Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY, USA
Shu-Fu Lin, email: email@example.com
Keywords: roniciclib, cyclin-dependent kinase, anaplastic thyroid cancer
Received: March 02, 2017 Accepted: May 23, 2017 Published: July 08, 2017
Many human cancers have altered cyclin-dependent kinase activity. Inhibition of cyclin-dependent kinases may arrest cell cycle progression and represents an important strategy in the treatment of malignancies. We evaluated the therapeutic effects of roniciclib, a cyclin-dependent kinase inhibitor, as a treatment for anaplastic thyroid cancer. Roniciclib inhibited anaplastic thyroid cancer cell proliferation in a dose-dependent manner. Roniciclib activated caspase-3 activity and induced apoptosis. Cell cycle progression was arrested in G2/M phase. In vivo, the growth of anaplastic thyroid cancer xenograft tumors was retarded by roniciclib treatment without evidence of toxicity. These data provide a rationale for further clinical evaluation using roniciclib in the treatment of patients with anaplastic thyroid cancer.
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