Intestinal epithelial TRE-Msi1
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE74321 | GEO | 2015/10/24
SECONDARY ACCESSION(S): PRJNA299662
REPOSITORIES: GEO
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Project description:Comparison of gene expression in intestinal epithelial cells in the presence or absence of ectopic induction of Msi1 in vivo Total RNA was isolated from preparations of total intestinal epithelial cells taken from the jejunum from 3 control (R26-M2rtTA +doxycycline for 24 hrs) and 3 experimental (TRE-Msi1::R26-M2rtTA +doxycycline for 24 hrs) animals and subjected to profiling on affymetrix Gene 1.0ST arrays
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Project description:Comparison of gene expression in intestinal epithelial cells in the presence or absence of ectopic induction of MSI2 in vivo Total RNA was isolated from preparations of total intestinal epithelial cells taken from the jejunum from 3 control (R26-M2rtTA +doxycycline for 24 hrs) and 3 experimental (TRE-MSI2::R26-M2rtTA +doxycycline for 24 hrs) and subjected to profiling on affymetrix Gene 1.0ST arrays
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Project description:Loss of the APC tumor suppressor in the intestinal epithelium initiates the majority of human colorectal adenocarcinomas. Constitutive β-catenin activation is thought to underlie tumorigenesis induced by loss of APC, however β-catenin activation alone does not recapitulate all APC-loss phenotypes, suggesting that additional pathways are required. We demonstrate that aberrant activation of the Msi1 RNA binding protein occurs upon APC loss and that constitutive Msi1 activation alone is sufficient to phenocopy APC loss in the intestinal epithelium. Msi1 elicits these effects through binding of mRNAs encoding pleiotropic tumor suppressors resulting in promiscuous activation of quiescent intestinal stem cells, proliferative expansion of the stem cell compartment, crypt fission, and blocked differentiation. Further, we find these phenotypes to be largely dependent on mTORC1 activity, and demonstrate that loss of Msi activity is sufficient to abrogate tumorigenesis in mouse and human systems. Our findings implicate Msi1 as a central coordinator of APC loss-induced intestinal stem cell transformation and adenocarcinoma progression. 2 wild-type, 2 transgenic samples
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Project description:Members of the Msi family of RNA-binding proteins have recently emerged as potent oncoproteins in a range of malignancies. MSI2 is highly expressed in hematopoietic cancers, where it is required for disease maintenance. In contrast to the hematopoietic system, colorectal cancers can express both Msi family members, MSI1 and MSI2. Here, we demonstrate that, in the intestinal epithelium, Msi1 and Msi2 have analogous oncogenic effects. Further, comparison of Msi1/2-induced gene expression programs and transcriptome-wide analyses of Msi1/2-RNA-binding targets reveal significant functional overlap, including induction of the PDK-Akt-mTORC1 axis. Ultimately, we demonstrate that concomitant loss of function of both MSI family members is sufficient to abrogate the growth of human colorectal cancer cells, and Msi gene deletion inhibits tumorigenesis in several mouse models of intestinal cancer. Our findings demonstrate that MSI1 and MSI2 act as functionally redundant oncoproteins required for the ontogeny of intestinal cancers.
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Project description:The translational reactivation of maternal mRNAs encoding the drivers of vertebrate meiosis is accomplished mainly by cytoplasmic polyadenylation. The Cytoplasmic Polyadenylation Elements (CPEs) present in the 3’ UTR of these transcripts, together with their cognate CPE-binding proteins (CPEBs), define a combinatorial code that determines the timing and extent of translational activation upon meiosis resumption. In addition, the RNA-binding protein Musashi1 (Msi1) regulates the polyadenylation of CPE-containing mRNAs by an as yet undefined CPEB-dependent or -independent mechanism. Here we show that Msi1 alone does not support cytoplasmic polyadenylation, but its binding triggers the remodeling of RNA structure, thereby exposing adjacent CPEs and stimulating polyadenylation. Thus, Msi1 directs the preferential use of specific CPEs, which in turn affects the timing and extent of polyadenylation during meiotic progression. Genome-wide analysis of CPEB1- and Msi-associated mRNAs identified 491 common targets, thus revealing a new layer of CPE-mediated translational control.
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Project description:RIP-Chip analysis of Msi1 and identification of preferentially associated mRNAs. Keywords: RIP-Chip
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Project description:Musashi1 (Msi1) is a highly conserved RNA binding protein that is required during the development of the nervous system. Msi1 has a role in neural stem cells, controlling the balance between self-renewal and differentiation. Msi1 has also been implicated in cancer, being highly expressed in multiple tumor types. In this study, we analyzed Msi1 expression in a large cohort of medulloblastoma samples and showed that Msi1 is highly expressed in tumor tissue compared to normal cerebellum and that high Msi1 expression is associated with a poor prognosis. Using a nude mouse xenograft model, we demonstrate that Msi1 is important for tumor growth. We then used RIP-chip (ribonucleoprotein immunoprecipitation followed by microarray analysis) to identify mRNA targets of Msi1 in medulloblastoma. In conclusion, our results suggest that Msi1 functions as a regulator of multiple processes in medulloblastoma formation and could become an important therapeutic target.
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