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Fig. 5 | BMC Cancer

Fig. 5

From: Epigenetic loss of heterozygosity of Apc and an inflammation-associated mutational signature detected in Lrig1+/−-driven murine colonic adenomas

Fig. 5

The adenomas selectively express mutated adenomatous polyposis coli (Apc) transcripts originating from a recombined transgene. The epigenetic loss of heterozygosity of Apc was apparent in the mRNA of the adenomas, which are missing exon 15 from Apc mRNA transcripts. RNA sequencing reads from adjacent nontumor tissue (top three rows) and adenoma (bottom five rows) are shown. The putative mechanism of Apc loss in these adenomas appears to proceed via epigenetic silencing of the wild-type allele and selective transcription of the mutant Apc gene, which lacks exon 15 after Cre recombinase- induced recombination under the control of the leucine-rich repeats and immunoglobulin-like domains 1 (Lrig1) promoter. The purity of the tumor samples is demonstrated by the complete lack of Apc exon 15 from tumors T10, T11, and T12. Tumors T13 and T14, which have retained some expression of Apc exon 15, were found to have gene expression patterns most similar to wild-type cells based on RNA-Seq

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