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. 2014 May 13;5(11):3611–3621. doi: 10.18632/oncotarget.1968

Figure 5. CAMK2N1 suppresses IGF-1, ErbB2, VEGF, downstream kinase-PI3K/AKT, MEK/ERK and HSP27-mediated signaling pathways in prostate cancer cells.

Figure 5

(A-B) Microarray gene expression analysis was conducted in DU145 cells stably overexpressing CAMK2N1 (>1.5-fold and p < 0.05). (A) Functional analysis of differentially expressed genes. Gene Ontology (GO) Biological Process (BP) terms were ranked by score (score > 1.3). (B) CAMK2N1 induced and repressed clusters of genes that were chosen from the pathways. (C-D) Expression levels of ErbB2, AKT, MEK1, ERK1/2, NFκβ, Bcl-2, BAX, and p21 were determined by Western blot in DU145 cells with stably overexpressing CAMK2N1. Similar changes as to those found in the microarray analysis were observed. Each figure represents three independent experiments. (E) DU145 tumors stably expressing CAMK2N1, and mRNA levels of ErbB2, Bcl-2, NF-κβ, AKT1, AR, p21, and Bax were determined by qRT-PCR. CAMK2N1 decreased ErbB2, BCL-2, NF-κβ, AKT1, AR mRNA levels and increased p21, Bax mRNA levels in DU145 tumor tissues. The data is shown as mean ± SEM for N=4 separate tumors for each group.