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Inhibition of KIF20B sensitizes hepatocellular carcinoma cell to microtubule-targeting agents by blocking cytokinesis.

著者 Liu X , Li Y , Zhang X , Liu XY , Peng A , Chen Y , Meng L , Chen H , Zhang Y , Miao X , Zheng L , Huang K
Cancer Sci.2018 Sep 06 ; ():.
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Kinesin family member 20B (KIF20B, also known as MPHOSPH1) is a kinesin protein which plays a critical role in cytokinesis. Previously, we and others have demonstrated the oncogenic role of KIF20B in several cancers; however, the exact mechanisms underlying its tumorigenic effects remain unclear. Here we showed overexpression of KIF20B in human hepatocellular carcinoma (HCC), and reported a negative correlation between KIF20B level and prognosis of patients. Mechanistically, reducing KIF20B blockades mitotic exit of HCC cells at telophase in a spindle assembly checkpoint independent manner. Importantly, reducing KIF20B acts synergistically with three microtubule-associated agents (MTAs) to p53- or p14ARF-dependently suppress p53-wt or p53-null HCC cells. In addition to taxol, reducing KIF20B also enhanced the toxicity of two chemotherapeutic drugs, hydroxycamptothecin and mitomycin C. In conclusion, we found a novel mechanism that blocking cytokinesis by KIF20B inhibition increases the efficacy of MTAs; our results thus suggested a dual-mitotic suppression approach against HCC by combining MTAs with KIF20B inhibition, which simultaneously blocks mitosis at both metaphase and telophase. This article is protected by copyright. All rights reserved.
PMID: 30191636 [PubMed - as supplied by publisher]
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