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. 2020 Aug 31;12(9):2467. doi: 10.3390/cancers12092467

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Resistance phenotype of ADT resistant PCa cells. Cell number was determined on days 0, 3, 6 and 10 post treatment with (a) hormone ablation, (b) 10 µM abiraterone acetate, (c) 40 µM apalutamide, or (d) 20 µM enzalutamide. Cells used are LNCaP (LNCaP-wt) cells, and their resistant sublines to: hormone ablation (LNCaP-abl), abiraterone acetate (LNCaP-abi), or apalutamide (LNCaP-ARN509), as well as wildtype C4-2B (C4-2B-wt) cells, or their resistant subclone to enzalutamide (C4-2B-ENZA). Cell-doubling time was calculated for each treatment by fitting exponential growth curves using GraphPad Prism 7. Shown are means ±SEM of at least three independent experiments. Significance is indicated as * for the p < 0.05, 0.001 and *** for p < 0.0001, ns: not significant.

Resistance phenotype of ADT resistant PCa cells. Cell number was determined on days 0, 3, 6 and 10 post treatment with (a) hormone ablation, (b) 10 µM abiraterone acetate, (c) 40 µM apalutamide, or (d) 20 µM enzalutamide. Cells used are LNCaP (LNCaP-wt) cells, and their resistant sublines to: hormone ablation (LNCaP-abl), abiraterone acetate (LNCaP-abi), or apalutamide (LNCaP-ARN509), as well as wildtype C4-2B (C4-2B-wt) cells, or their resistant subclone to enzalutamide (C4-2B-ENZA). Cell-doubling time was calculated for each treatment by fitting exponential growth curves using GraphPad Prism 7. Shown are means ±SEM of at least three independent experiments. Significance is indicated as * for the p < 0.05, 0.001 and *** for p < 0.0001, ns: not significant.