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Fig. 7 | Cell Communication and Signaling

Fig. 7

From: Impairment of IGF2 gene expression in prostate cancer is triggered by epigenetic dysregulation of IGF2-DMR0 and its interaction with KLF4

Fig. 7

Enrichment of KLF4 in IGF2-DMR0 depends on IGF2-DMR0 methylation and affects the IGF2-mRNA expression. a Chromatin immunoprcipitation analyses revealed a high enrichment of KLF4 in IGF2-DMR0 in LNCaP cells (17% methylated in IGF2-DMR0) and low enrichment in DU145 cells (85% methylated in IGF2-DMR0). Treatment of DU145 cells with 5-Aza (DU145 + 5-aza) led to an increase of KLF4 binding in IGF2-DMR0. b Untreated (control) prostate cancer cell lines LNCaP and DU145 showed similar low levels of IGF2 expression. Treatment with DNA methyltransferase inhibitor 5-aza-2′-deoxycytidin (5-Aza) caused a strong increase of IGF2-mRNA expression in DU145 cells, whereas LNCaP cells were unaffected. c Prostate tissue samples from TUR-BPH, RP-BPH and RP-PCa were analyzed regarding the KLF4-mRNA expression. No significant differences were found between the groups. d A highly significant positive correlation between KLF4 and IGF2 expression (Spearman’s rank correlation coefficient r = 0.668, p < 0.0001) was found, when all analyzed primary tumors were considered together without splitting in separate groups

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