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Tumor suppression by miR-26 overrides potential oncogenic activity in intestinal tumorigenesis

ABSTRACT: Through a series of mouse genetic studies, we concluded that miR-26 overexpression in intestinal epithelial cells inhibits tumor formation in Apcmin/+ mice. We isolated intestinal epithelial cells from M2rtTA and M2rtTA; eGFP.miR-26a to assess gene expression changes after the induction of miR-26a expression.

ORGANISM(S): Mus musculus

PROVIDER: GSE62831 | GEO | 2014/10/30

SECONDARY ACCESSION(S): PRJNA265491

REPOSITORIES: GEO

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Tumor suppression by miR-26 overrides potential oncogenic activity in intestinal tumorigenesis

Project description:Through a series of mouse genetic studies, we concluded that miR-26 overexpression in intestinal epithelial cells inhibits tumor formation in Apcmin/+ mice. We isolated intestinal epithelial cells from M2rtTA and M2rtTA; eGFP.miR-26a to assess gene expression changes after the induction of miR-26a expression. Intestinal epithelial cells were isolated from three M2rtTA and three M2rtTA; eGFP.miR-26a mice after treatment with doxycycline for 10 days. Gene expression was profiled using Illumina microarrays.

2014-10-30 | E-GEOD-62831 | biostudies-arrayexpress

Tumor suppression by miR-26 overrides potential oncogenic activity in intestinal tumorigenesis.

Project description:Down-regulation of miR-26 family members has been implicated in the pathogenesis of multiple malignancies. In some settings, including glioma, however, miR-26-mediated repression of PTEN promotes tumorigenesis. To investigate the contexts in which the tumor suppressor versus oncogenic activity of miR-26 predominates in vivo, we generated miR-26a transgenic mice. Despite measureable repression of Pten, elevated miR-26a levels were not associated with malignancy in transgenic animals. We documented reduced miR-26 expression in human colorectal cancer and, accordingly, showed that miR-26a expression potently suppressed intestinal adenoma formation in Apc(min/+) mice, a model known to be sensitive to Pten dosage. These studies reveal a tumor suppressor role for miR-26 in intestinal cancer that overrides putative oncogenic activity, highlighting the therapeutic potential of miR-26 delivery to this tumor type.

| S-EPMC4248289 | biostudies-literature

CSF1R mediates effects of miR-34a loss during intestinal tumorigenesis in ApcMin mice (adenoma)

Project description:To address the in vivo relevance of CSF1R regulation by miR-34a during intestinal tumor formation, we generated ApcMin/+ mice with intestinal-epithelial cell (IEC)-specific deletions of the Mir34a and/or Csf1r genes. The mRNA expression profiles of intestinal adenomas with and without functional miR-34a and/or Csf1r were compared.

2022-10-04 | GSE167448 | GEO

CSF1R mediates effects of miR-34a loss during intestinal tumorigenesis in ApcMin mice (tumor organoid)

Project description:To address the in vivo relevance of CSF1R regulation by miR-34a during intestinal tumor formation, we generated ApcMin/+ mice with intestinal-epithelial cell (IEC)-specific deletions of the Mir34a and/or Csf1r genes. The mRNA expression profiles of tumor organoids derived ffrom intestinal adenomas with and without functional miR-34a and/or Csf1r were compared.

2022-10-04 | GSE167449 | GEO

miR-34a and miR-34b/c suppress intestinal tumorigenesis in ApcMin/+ Mice

Project description:miR-34a and miR-34b/c genes are frequently epigenetically silenced in primary CRCs. However, the in vivo relevance of miR-34a/b/c for suppression of intestinal tumor formation has not been analyzed by genetic approaches. ApcMin/+ mice with deletion of the miR-34a and miR-34b/c genes were generated and analyzed. The mRNA expression profiles of intestinal adenomas with and without functional miR-34a/b/c genes were compared.

2017-05-28 | GSE84138 | GEO

Mouse Articular chondrocyte LC-MSMS of wild-type, miR-26a -/- and cartilage-specific miR-23ab clusters knockout mice

Project description:To reveal the potential regulation target genes of miR-26a and miR-23a/b clusters in articular chondrocytes, we performed a multi-omics analysis of LC-MSMS and RNA-seq using cultured chondrocytes samples, which were primarily isolated from 3-week-old wild-type, miR-26a -/- (with or without miR-26a mimic transfection afterwards) or miR-23a/b cluster flox/flox;Col2a1-cre mice. For LC-MSMS, protein from TRIZOL reagent was extracted, nanoLC-MSMS was performed. An expression list was made to further explore the regulation targets of miR-26a and miR-23a/b clusters.

2023-01-25 | PXD031868 | Pride

miR-26 suppresses adipocyte progenitor differentiation and fat production by targeting Fbxl19

Project description:Purpose: Fat storage in adult mammals is a highly regulated process that involves the mobilization of adipocyte progenitor cells (APCs) that differentiate to produce new adipocytes. Here we report an unexpected role for the broadly conserved miR-26 family of microRNAs (miR-26a-1, miR-26a-2, and miR-26b) as key regulators of APC differentiation. Global loss of miR-26 resulted in a dramatic expansion of adipose tissue in adult mice fed normal chow. Conversely, transgenic overexpression of miR-26a protected mice from high fat diet-induced obesity. These effects were attributable to a cell-autonomous function of miR-26 as a potent inhibitor of APC differentiation. miR-26 blocks adipogenesis, at least in part, by repressing expression of Fbxl19, a conserved miR-26 target without a previously known role in adipocyte biology that encodes a component of SCF-type E3 ubiquitin ligase complexes. These findings have therefore revealed a new pathway that plays a critical role in regulating adipose tissue formation in vivo and suggest new potential therapeutic targets for obesity and related disorders.

2020-01-21 | GSE134736 | GEO

Notch signaling suppresses the progression of colorectal tumorigenesis

Project description:The Notch signaling pathway regulates fate decision, proliferation and differentiation of intestinal epithelial cells. However, the role of Notch signaling in colorectal cancer progression is largely unknown. Here we show that Notch signaling suppresses the progression of colorectal tumorigenesis, even though it augments tumor initiation. In contrast to adenomas of Apcmin mice, Notch-inactivated Apcmin adenomas showed more malignant characteristics, such as submucosal invasion and loss of glandular pattern. Conversely, Notch-activated Apcmin adenomas showed a reversion from high-grade to low-grade features, such as the restoration of adherent junctions. Expression profiling revealed that Notch signaling promotes the differentiation of tumor cells with down regulation of Wnt/beta-catenin target genes and inhibition of epithelial-mesenchymal transition. Comparison of mouse and human expression profiles also suggests the common role of Notch in inhibition of tumor progression. Interestingly, Notch signaling suppressed the expression of beta-catenin responsive genes through chromatin modification of Tcf4/beta-catenin binding sides. Our results suggest that Notch signaling has dual roles in colorectal tumorigenesis: promoting adenoma initiation, while inhibiting tumor progression to colorectal cancer. mRNAs from normal (WT, Notch-activated and Notch-inactivated) and tumor (WT, Notch-activated and Notch-inactivated) tissues were profiled.

2011-04-19 | E-GEOD-21392 | biostudies-arrayexpress

Innate mesenchymal TLR4/MyD88 signals promote spontaneous intestinal tumorigenesis

Project description:This study shows that the TLR4/MyD88 pathway in intestinal mesenchymal cells promotes intestinal carcinogenesis in the APCmin mouse model.

2019-01-15 | GSE119341 | GEO

Effects of miR-26a expression and miRNA-sponge-mediated miR-26 family knockdown on the transcriptome of B cell precursors

Project description:Here, we have screened a miRNA expression library in a pre-B cell expression system to identify miRNAs with a potential oncogenic activity in early lymphocytes. We show that miR-26a is sufficient to transform B cell precursors in vitro as defined by growth factor independence, and demonstrate that its continuous expression is necessary to keep cells in the transformed state. Mechanistically, we find that expression of miR-26a protects against apoptosis induced by growth factor withdrawal as well as DNA damage, provides a competitve advantage and interferes with the differentiation of pre-B to immature B cells. In consequence, transformed cells express the pre-BCR on the cell surface, which appears to provide signals for ongoing proliferation and survival. Using microarray analysis, we identified several previously known and novel putative target genes of miR-26a in B cell precursors. A key target appears to be PTEN, a well established tumor suppressor and regulator of PI3K signaling, as knockdown of Pten mRNA by shRNA at least partially phenocopies miR-26a overexpression. To gain inside into the physiological role of miR-26 in early B cell develobment, in contrast to the oncogenic situation if aberrantly overexpressed, we further more sequestered endogenous miR-26a and b by expression of a miRNA sponge. This functional knockdown indeed induced the reciprocal phenotype relative to the overexpression, i.e. cells had a proliferative disadvantage and differentiated more efficient into immature B cells. Surprisingly, however, transcriptional changes induced by miR-26 sequestration were very mild. We therefoer hypothesize that most of the sponge-mediated deregulation is below detection level while still being functional relevant.

2022-01-01 | GSE186236 | GEO

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