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. Author manuscript; available in PMC: 2014 Mar 9.
Published in final edited form as: Mol Cell. 2007 Aug 3;27(3):380–392. doi: 10.1016/j.molcel.2007.05.041

Figure 7. Functional Roles of Collaborating Transcription Factors in Mediating the PDE9A Gene Transcription and Prostate Cancer Cell Proliferation.

Figure 7

(A) AR binding sites relative to the PDE9A gene. The black blocks represent AR binding sites. The PDE9A gene is shown in its 5′-3′ orientation, and the blue arrows indicate the direction of the gene (June 05, University of California, Santa Cruz [UCSC], known genes).

(B) Effects of FoxA1, GATA2, and Oct1 silencing on PDE9A mRNA expression. siRNA-RTPCR analyses were performed as described in Figure 6B.

(C) Effects of silencing GATA2 and Oct1 on AR, Pol II, Oct1, and GATA2 recruitment to the PDE9A enhancers. siRNA-ChIP analyses were performed as described in Figure 6C.

(D) Effects of AR and cofactor silencing on androgen-stimulated cell cycle entry. Forty-eight hours after siRNA transfection, cells were treated with or without 1 or 10 nM DHT for 24 hr. Cells were then fixed, stained with propidium iodide, and analyzed by flow cytometry. Values represent the mean ± SE of two to three independent experiments (B) to (D).