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RNA splicing is a key mediator of tumour cell plasticity and a therapeutic vulnerability in colorectal cancer [Apc mutant and Apc Srsf1 double mutant]

ABSTRACT: RNA splicing is a key mediator of tumour cell plasticity and a therapeutic vulnerability in colorectal cancer [Apc mutant and Apc Srsf1 double mutant]

PROVIDER: PRJNA820781 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18507000_1.fastq.gz	Fastqsanger.gz
	SRR18507000_2.fastq.gz	Fastqsanger.gz
	SRR18507001_1.fastq.gz	Fastqsanger.gz
	SRR18507001_2.fastq.gz	Fastqsanger.gz
	SRR18507002_1.fastq.gz	Fastqsanger.gz

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RNA splicing is a key mediator of tumour cell plasticity and a therapeutic vulnerability in colorectal cancer [Apc mutant and Apc Srsf1 double mutant]

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Apc-mutants act as supercompetitors in intestinal tumour initiation

Project description:Almost all colorectal cancers (CRC) present with mutations in the Apc gene, leading to unrestrained Wnt activation and the initiation of tumour development. We previously reported the competitive benefit of Apc-mutant intestinal stem cells (ISCs) within the crypt, however, the mechanism by which they outcompete their wild type (WT) neighbours remained elusive. Here, we studied the effect of Apc-mutants using an in vitro culture system of WT (Lgr5-CreErt2) and Apc-/- (Lgr5-CreErt2;Apcfl/fl) organoids . The expression patterns of WT and Apc-/- organoids revealed significant upregulation in specific secreted Wnt antagonists Notum, Wif1 and Dkk2. Furthermore, we studied the effect of the secreted antagonist by treating WT organoids with either WT or Apc-/- conditioned medium (CM) for 48 hours and observed a significant decrease in stem cell markers and an increase in goblet cell markers. We report that Apc-mutants act as bona fide supercompetitors by secreting Wnt antagonists that result in active differentiation of WT ISCs.

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Project description:APC is a classical tumor suppressor in humans, and truncating mutations are early somatic events in most cases of sporadic colon cancer. APC directly enhances the activity of glycogen synthase kinase 3 (GSK-3) and therefore loss of full length APC reduces GSK-3 activity, leading to stabilization of b-catenin protein and activation of downstream Wnt/b-catenin signaling. GSK-3 also phosphorylates multiple core mRNA splicing factors and loss of Gsk3a/b in mouse ES cells and human lymphocytes alters mRNA splicing at a genome wide level. We therefore predict that loss of APC should similarly alter splicing by reducing GSK-3 activity. Here we use RNA-seq to assess differential gene expression and altered splicing in apc-mcr mutant zebrafish embryos at 48hpf. We find robust activation of known Wnt/b-catenin target genes, as expected. Surprisingly, we also find markedly increased expression of multiple genes related to inflammation and cytokine signaling. We also identify 340 mRNA splicing variations in apc mutant zebrafish. Many of these local splice variants (LSVs) occur in mRNAs the regulate cell adhesion, migration, and morphogenesis.

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