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Article Publish Status: FREE
Abstract Title:

Targeting Aurora B kinase with Tanshinone IIA suppresses tumor growth and overcomes radioresistance.

Abstract Source:

Cell Death Dis. 2021 Feb 4 ;12(2):152. Epub 2021 Feb 4. PMID: 33542222

Abstract Author(s):

Ming Li, Haidan Liu, Qin Zhao, Shuangze Han, Li Zhou, Wenbin Liu, Wei Li, Feng Gao

Article Affiliation:

Ming Li

Abstract:

Aurora B kinase is aberrantly overexpressed in various tumors and shown to be a promising target for anti-cancer therapy. In human oral squamous cell carcinoma (OSCC), the high protein level of Aurora B is required for maintaining of malignant phenotypes, including in vitro cell growth, colony formation, and in vivo tumor development. By molecular modeling screening of 74 commercially available natural products, we identified that Tanshinone IIA (Tan IIA), as a potential Aurora B kinase inhibitor. The in silico docking study indicates that Tan IIA docks into the ATP-binding pocket of Aurora B, which is further confirmed by in vitro kinase assay, ex vivo pull-down, and ATP competitive binding assay. Tan IIA exhibited a significant anti-tumor effect on OSCC cells both in vitro and in vivo, including reduction of Aurora B and histone H3 phosphorylation, induction of G2/M cell cycle arrest, increase the population of polyploid cells, and promotion of apoptosis. The in vivo mouse model revealed that Tan IIA delayed tumor growth of OSCC cells. Tan IIA alone or in combination with radiation overcame radioresistance in OSCC xenograft tumors. Taken together, our data indicate that Tan IIA is an Aurora B kinase inhibitor with therapeutic potentials for cancer treatment.

Study Type : In Vitro Study

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