**5. Conclusions**

In summary, we demonstrated that KLF5 is crucial for androgen/AR signaling to activate the transcription of specific genes, including some that mediate cell proliferation, and to promote cell proliferation and tumor growth in PCa cells. Mechanistically, androgen promotes the expression of KLF5 via AR, KLF5 in turn promotes the transcription of AR by binding to AR promoter, and KLF5 and AR coordinate to transactivate the target genes of AR. These findings not only suggest that KLF5 is a crucial factor for the function of AR in PCa cells, they will also further the understanding of how AR signaling is sustained in CRPC. In addition, they will likely facilitate the development of therapeutic strategies for the treatment of CRPC.

**Supplementary Materials:** The following are available online at http://www.mdpi.com/2072-6694/12/3/748/s1, Figure S1: Unprocessed blot images for western blotting results, Table S1: Primer sequences used in various PCRs in the study.

**Author Contributions:** Data curation, J.L. and J.A.; Funding acquisition, J.-T.D.; Investigation, J.L., M.L., X.F. and X.C.; Methodology, B.Z., M.L., X.F., X.C., C.F., G.D., R.W., Z.Z. and L.F.; Writing – original draft, J.L.; Writing – review & editing, B.Z., Z.Z. and J.-T.D. All authors have read and agreed to the published version of the manuscript.

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

**Acknowledgments:** We thank Anthea Hammond of Emory University for editing the manuscript. We also thank Qiao Wu, Gui Ma and Qingxia Hu, Xiawei Li, and Na An of Nankai University for advice and help throughout the study.

**Conflicts of Interest:** All authors declare no conflict of interest to this work.
