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. Author manuscript; available in PMC: 2016 May 1.
Published in final edited form as: Mol Cancer Res. 2015 Feb 20;13(5):828–838. doi: 10.1158/1541-7786.MCR-15-0016-T

Figure 7. Schematic representation of the proposed regulation of lncRNA cluster, DRAIC/PCAT29.

Figure 7

(A) Comparison of DRAIC and PCAT29. (B) In AD cells, even though AR activated by androgen is recruited to DRAIC/PCAT29 cluster to repress these two lncRNA, the high level of FOXA1 counters the repression of DRAIC/PCAT29 by AR and induces the transcription of these lncRNAs. NKX3-1, which is indirectly up-regulated by FOXA1, contributes to the induction of DRAIC/PCAT29. During tumor progression, the expression of FOXA1 and NKX3-1 is downregulated and AR pathways are differentially activated despite low androgen in CR cells. The decrease of FOXA1 enhances AR recruitment to the cluster and represses DRAIC/PCAT29. ADT selects for cells with decreased DRAIC expression. The decrease of tumor suppressive lncRNAs, DRAIC and PCAT29, leads to higher invasion ability and lower disease free survival in prostate cancer patients.