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. Author manuscript; available in PMC: 2010 Dec 1.
Published in final edited form as: Cancer Res. 2009 Nov 3;69(23):9038–9046. doi: 10.1158/0008-5472.CAN-09-1499

Figure 3.

Figure 3

Reactivation of miR-129-2 in cancer cells by pharmacological induction of hyperacetylation and DNA demethylation lead to reduced SOX4 expression at both the mRNA and protein levels. A, genomic map of miR-129-2 CpG island and amplicon. Bar under line, CpG site; ↓, AciI cutting sites. B, COBRA analysis in endometrial cancer cell lines. u, unmethylated band; m, methylated bands; SssI, 100% methylated control; Blood, a mix of 4 normal peripheral blood samples as negative control; +, AciI restriction enzyme added; -, without AciI. C, relative expression levels of miR-129-3p in endometrial cancer cell lines treated with DAC and/or TSA in relation to untreated controls was determined by RT-qPCR analysis. RNU48 was used as internal control gene. Error bar, SD; *, P < 0.05 compared with untreated control of the same cell type. D, relative expression levels of SOX4 mRNA (right) and protein (right) indicating a down-regulation of SOX4 in endometrial cancer cells after treatment with DAC and/or TSA. GAPDH or β-actin was used as internal or loading control, respectively.