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. 2020 May 22;117(23):13012–13022. doi: 10.1073/pnas.1918845117

Fig. 5.

Fig. 5.

KRAS mutation down-regulates MATE1 through mediating the hypermethylation status on the CpG island of the MATE1 promoter. (A) The correlation between MATE1 transcriptional levels and methylation levels of CpG sites on the promoter of MATE1. Data from TCGA-COAD RNA-seq-HTseq-FPKM-521 (workflow type HTSeq-FPKM, normalized from RNA-seq of 521 samples) and methyArray 450k were conducted by Pearson’s correlation analysis. (B) Bisulfite sequencing PCR analysis showing the methylation status of CpG sites on the MATE1 promoter in CRC cell lines. (C) Immunoblot analysis of MATE1 levels and BSP analysis of the MATE1 promoter are shown between KRASG13D SW48 and its counterpart SW48. (D) Immunoblot analysis monitoring MATE1 levels and CpG-site methylation on the MATE1 promoter in KRAS shRNA-LoVo cells treated with dimethyl sulfoxide (DMSO) as a negative control or azacitidine as a positive control. (E) The MATE1 expression in 374469 KRASWT colon adenocarcinoma and 386650 KRASG12D colon mucinous adenocarcinoma was analyzed by immunoblot, and the methylation status of CpG sites on the MATE1 promoter was determined by BSP. Data are shown as mean ± SEM. All P values were determined by two-way ANOVA. *P < 0.05, **P < 0.01.