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. 2019 May 8;11:1758835919846375. doi: 10.1177/1758835919846375

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© The Author(s), 2019

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 8. — Plausible model of cotargeting Plk1 and androgen receptor (AR) in paclitaxel-resistant prostate cancer. (a) Although paclitaxel-resistant cancer cells acquired resistance to paclitaxel, they are still sensitive to Plk1 inhibitors, which may be due to the inhibitory effect on the expression and activity of Plk1. (b) Paclitaxel-resistant prostate cancer cells showed high mRNA levels of AR and prostate-specific antigen (PSA) compared with those of the parental cells, which is downregulated by the AR antagonist bicalutamide. Based on these plausible mechanisms, cotargeting Plk1 and AR would be effective in the treatment of advanced prostate cancer.