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. 2020 Oct 20;14(1):100915. doi: 10.1016/j.tranon.2020.100915

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© 2020 Published by Elsevier Inc.

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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Fig 5 — SLC3A2 expression in clinical datasets. . (A) Epigenetic status around SLC3A2. AR/AR-V7 binding to SLC3A2 enhancer and elevated level of H3K27ac signal in LNCaP95 in the absence and presence of DHT were shown. (B) RNA expression of SLC3A2. AR-V7 knockdown decreased FPKM value of SLC3A2. (C) FAIRE-qPCR analysis at AR/AR-V7 target region around SLC3A2 in hormone-depleted or -stimulated LNCaP and hormone-depleted LNCaP95. (D) RT-qPCR analysis of SLC3A2 in LNCaP and LNCaP95 cells with/without shRNA treatment. Downregulation of SLC3A2 by AR-V7 knockdown was confirmed. (E) Reduction of H3K27ac level at the SLC3A2 enhancer. H3K27ac enrichment was measured by ChIP-qPCR at AR/AR-V7 target region around SLC3A2, showing a decrease following AR-V7 knockdown. (F)SLC3A2 expression levels in benign lesions, primary PC, and CRPC, using Grasso prostate dataset. (G)SLC3A2 expression levels in PC cases with higher and lower expression of AR-V7, using TCGA PRAD dataset.