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

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

PROVIDER: PRJNA820859 | ENA |

REPOSITORIES: ENA

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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]

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

| PRJNA820781 | ENA

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

Project description:mRNAseq of Apc mutant and Apc Srsf1 double mutant mouse small intestine.

2022-03-31 | GSE199600 | GEO

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

Project description:mRNAseq of wild-type and Apc mutant mouse small intestine.

2022-03-31 | GSE199622 | GEO

RNA splicing is a key mediator of tumour cell plasticity and a therapeutic vulnerability in colorectal cancer

Project description:RNA splicing is a key mediator of tumour cell plasticity and a therapeutic vulnerability in colorectal cancer

| PRJNA820858 | ENA

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.

2021-03-25 | GSE144325 | GEO

Apc-mutants act as supercompetitors in intestinal tumour initiation

Project description:Apc-mutants act as supercompetitors in intestinal tumour initiation

| PRJNA603370 | ENA

RNA splicing is a key mediator of tumour cell plasticity and a therapeutic vulnerability in colorectal cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-03-31 | GSE199623 | GEO

APC and P53 mutations synergize to create a therapeutic vulnerability to NOTUM inhibition in advanced colorectal cancer [bulk RNA-seq]

Project description:We report that inactivation of the APC tumor suppressor results in dramatic activation of the NOTUM carboxylesterase, which has potent tumor suppressive activity in APC-null adenomatous epithelium. During progression to adenocarcinoma, APC and TP53 mutations (usually coincident in advanced CRC) synergize, converting NOTUM to an obligate oncoprotein. We provide evidence that the Jekyll-and-Hyde behavior of NOTUM results from its differential activity upon enzymatic targets Glypicans 1 and 4 in early vs. late-stage disease, respectively. Ultimately, we demonstrate that small molecule inhibition of NOTUM activity in a mouse model of metastatic colon cancer is sufficient to arrest primary tumor growth and metastatic colonization. Thus, the extracellular carboxylesterase NOTUM represents a novel therapeutic vulnerability in advanced colorectal adenocarcinomas.

2022-12-31 | GSE198757 | GEO

A USP28-∆Np63 axis is a druggable vulnerability of squamous tumour formation and maintenance

Project description:A USP28-∆Np63 axis is a druggable vulnerability of squamous tumour formation and maintenance

| PRJNA533329 | ENA

APC and P53 mutations synergize to create a therapeutic vulnerability to NOTUM inhibition in advanced colorectal cancer [scRNA-seq]

Project description:We thought the immediate effects of APC inactivation may represent unexplored therapeutic vulnerabilities in later stages of advanced colorectal adenocarcinoma. We performed transcriptome profiling of epithelial colon organoids immediately after APC inactivation and cross-referenced gene expression changes to the transcriptomes of several mouse models of colon cancer, including colon tumors in an inflammation-induced CRC model (AOM-DSS), a model of familial adenomatous polyposis (FAP, the Apcmin mouse), and an implantation-based model of metastatic adenocarcinoma using Apc/Trp53/KrasG12D/Smad4 quadruple-mutant tumor organoids15 (APKS tumoroids). Of the roughly 150 genes whose expression is acutely induced upon APC loss and remains elevated in these colon cancer models.

2022-12-31 | GSE198758 | GEO

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