Inactivation of tumor-suppressor genes by DNA methylation has been found at high frequency in various cancers, suggesting that not only genetic changes but also epigenetic changes could contribute to development of cancer. Organoids derived from epithelial tumors have recently been utilized as a preclinical model in basic and translational studies. Although their reproducibility of in vivo environment attracts increasing attention in cancer research and toxicity assessment, however, it has not been clearly demonstrated whether the epigenetic status is maintained in organoids.Therefore, we performed whole genome DNA methylation analysis of colon and colon-derived organoids from F1 mouse (JF1 x C57BL/6J) crosses to evaluate if the organoids could faithfully reproduce the epigenetic status in vivo. Imprinted DMRs are good target to analyze, because it has been reported that imprinted DMRs of two parental alleles display reciprocal methylation patterns in vivo. By using SNPs in JF1 and C57BL/6J to distinguish paternal and maternal alleles, we found that DMRs in all existing imprinted region maintained in the organoids. Therefore, it might be possible that at least colon-derived organoids could faithfully reproduce the epigenetic status in vivo, suggesting that organoids would be a good model in cancer research and toxicity assessment.
