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Kinesin family member 20B ( KIF 20B, also known as  MPHOSPH 1) is a kinesin protein that plays a critical role in cytokinesis. Previously, we and others have demonstrated the oncogenic role of  KIF 20B in several cancers; however, the exact mechanisms underlying its tumorigenic effects remain unclear. Herein, we showed overexpression of  KIF 20B in human hepatocellular carcinoma ( HCC ) and reported a negative correlation between  KIF 20B level and prognosis of patients. Mechanistically, reducing  KIF 20B blockades mitotic exit of  HCC  cells at telophase in a spindle assembly checkpoint independent way. Importantly, reducing  KIF 20B acts synergistically with three microtubule‐associated agents ( MTA ) to p53‐ or p14 ARF ‐dependently suppress p53‐wt or p53‐null  HCC  cells. In addition to taxol, reducing  KIF 20B also enhanced the toxicity of two chemotherapeutic drugs, hydroxycamptothecin and mitomycin C. In conclusion, we found a novel mechanism in that blocking cytokinesis by  KIF 20B inhibition increases the efficacy of  MTA ; our results thus suggested a dual‐mitotic suppression approach against  HCC  by combining  MTA  with  KIF 20B inhibition, which simultaneously blocks mitosis at both metaphase and telophase.

Inhibition of kinesin family member 20B sensitizes hepatocellular carcinoma cell to microtubule‐targeting agents by blocking cytokinesis