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. 2017 Jun 7;8(32):53244–53261. doi: 10.18632/oncotarget.18387

Figure 3. CXCL13 was a novel downstream target gene of AR.

Figure 3

(A and B) LNCaP (A) and CWR22Rv1 (B) cells were transfected with siAR (AR siRNA)/control siRNA (Ctrl siRNA) and then treated with or without 10 nM Mib. Cells were harvested for western-blot assay to examine the protein levels of CXCL13, AR and β-actin. Knockdown of AR induced down-regulation of CXCL13 in both cell lines. (C and D) LNCaP cells (C) and PC3 cells (D) were transfected with AR, AR-N (a constitutively active isoform) and control vector pcDNA3.1(+). Cells were harvested for western-blot assay to examine the protein levels of CXCL13, AR and β-actin. Over-expression of AR and AR-N induced up-regulation of CXCL13 in both cell lines. (E and F) LNCaP cells (E) and CWR22Rv1 cells (F) were separately transfected with FOXO1, HDAC1 and pcDNA3.1(+) and then stimulated with 10 nM Mib as indicated. Cells harvested for western-blot assay to examine the protein levels of CXCL13, AR, FOXO1, HDAC1 and β-actin. Over-expression of FOXO1 and HDAC1 induced down-regulation of CXCL13, but no effect on AR. These experiments were repeated at least three times.