**5. Conclusions**

In conclusion, we used DTX-resistant PCa cell lines to analyze the role of KIFC1 in DTX resistance. We found that the expression of KIFC1 was significantly upregulated in cells with DTX resistance. Inhibition of KIFC1 induced an apoptosis pathway and re-sensitized the cellular response to DTX. Additionally, CW069 re-sensitized DTX-resistant cells to DTX treatment. The data presented here emphasize the grea<sup>t</sup> potential of combination therapy with DTX and CW069 in the treatment of PCa.

**Author Contributions:** Y.S., N.S., N.O., K.S., and W.Y. designed the study. Y.S., J.T., M.S., and A.M. provided patients' clinical information. Y.S. and Y.K. performed the experiments and acquired data. Y.S., N.S., N.O., and W.Y. interpreted the results. Y.S., N.O., and M.S. drafted the manuscript. N.O., J.T., A.M., K.S., and W.Y. edited it. All authors approved the final content for journal submission and publication.

**Funding:** This work was supported by Grants-in-Aid for Scientific Research (B) (15H04713) and for Challenging Exploratory Research (26670175, 16K15247) from the Japan Society for the Promotion of Science.

**Acknowledgments:** We thank M. Gleave (Vancouver Prostate Centre, Vancouver, BC, Canada) for originally providing the C4-2 cells. This work was carried out with the kind cooperation of the Research Center for Molecular Medicine of the Faculty of Medicine of Hiroshima University. We also thank the Analysis Center of Life Science of Hiroshima University for the use of their facilities.

**Conflicts of Interest:** The authors declare no conflict of interest.
