Fig. 2: SCNN1B promoter hypermethylation mediates its transcriptional silence and is associated with patient survival. | Oncogene

Fig. 2: SCNN1B promoter hypermethylation mediates its transcriptional silence and is associated with patient survival.

From: The sodium channel subunit SCNN1B suppresses colorectal cancer via suppression of active c-Raf and MAPK signaling cascade

Fig. 2

A The design of bisulfite genomic sequencing (BGS) and methylation-specific PCR (MSP) for SCNN1B promoter region. B RT-PCR and MSP of 10 CRC cell lines and 4 normal colon tissues. SCNN1B mRNA is silenced in CRC, concomitant with marked promoter hypermethylation. C DNA demethylation reagent, 5-Aza, restored SCNN1B mRNA in CRC cell lines. D BGS confirmed SCNN1B promoter hypermethylation in CRC cells as compared to normal colon. SCNN1B is hypermethylated in CRC tumor tissues as compared to paired adjacent normal colon tissues. E Analysis of TCGA CRC cohort (DNA methylation) showed that SCNN1B is hypermethylated in paired samples (left) and the overall cohort (right). F Integration of RNA-seq and DNA methylation in TCGA cohort revealed that SCNN1B expression is negatively correlated with its promoter methylation. G Kaplan-Meier curve analysis showed that high SCNN1B promoter hyper-methylation predicts poor survival of CRC patients (left), including early-stage (middle) and late-stage (right) CRC. H Univariate and multivariate Cox regression analysis validated SCNN1B as an independent prognostics factor for poor survival in CRC.

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