**5. Conclusions**

In summary, we have demonstrated that docetaxel-resistant LNCaP95 cells are cross-resistant to cabazitaxel. We showed that resistance to docetaxel and cabazitaxel depended on the increased expression of P-gp and the inhibition of P-gp with tariquidar restored to docetaxel and cabazitaxel. Furthermore, expression of AR-V7-regulated genes was increased in LNCaP95-DR cells, although AR-V7 did not contribute to taxane resistance. Finally, EPI-002, an antagonist of AR-NTD, inhibited proliferation of LNCaP95-DR. In conclusion, the present study described a potential option for the treatment of docetaxel-resistant, AR-V7-driven CRPC.

**Author Contributions:** Conceptualization, M.K. and M.D.S.; Methodology, M.K.; Software, Y.S.; Validation, Y.S., Y.T., Y.H., M.K. and M.D.S.; Formal Analysis, M.K.; Investigation, Y.S.; Resources, M.D.S.; Data Curation, S.T.; Writing—Original Draft Preparation, Y.S.; Writing—Review & Editing, M.K.; Visualization, T.I.; Supervision, T.N.; Project Administration, M.K.; Funding Acquisition, M.K. and M.D.S.

**Funding:** This research received no external funding.

**Acknowledgments:** This work was supported by the US National Cancer Institute (#R01 CA105304) awarded to MD Sadar and Grants–in–Aid for Scientific Research (JP16K20156) awarded to M.K.

**Conflicts of Interest:** M.D.S. receives compensation as a director, officer and consultant of ESSA Pharma Inc with stock equity. No potential conflicts of interest were disclosed for the other authors.
