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. 2016 Oct 25;7(48):78859–78871. doi: 10.18632/oncotarget.12889

Figure 1. NID2 is identified as a candidate gene in NPC and ESCC.

Figure 1

(A) The average methylation level of NID2 derived from our previous methylome data in NPC and ESCC. The vertical broken line shows the region covering the promoter CpG island (chr14: 52534582–52536722) and the bottom figures show a close-up view of changes in methylation. Methylation level is presented as β value (β = M/(U+M+100), M: signal intensity of the methylated allele, U: signal intensity of the unmethylated allele). The y-axis shows the average methylation level in tumors (orange line) and non-cancer controls (blue line), respectively. Within this region, the methylation levels in multiple CpG sites of both NPC and ESCC patients are consistently higher than those of non-cancer controls, with adjusted p value < 0.05 estimated by LIMMA analysis using the transformed β values as previously described [16]. Significance level of each selected probes were shown in Supplementary Figure S 1. (B) MMCT of chromosome 14 was previously performed using HONE1 as the recipient cell line [18]. qPCR analysis of tumor-suppressive microcell hybrids (MCHs) and their tumor segregant (TS) cell lines, which are no longer tumor-suppressive, showed that NID2 expression was down-regulated in all five TS cell lines, when compared to their respective MCHs. Asterisk (*) indicates samples with more than two-fold differences compared to its MCHs.