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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. 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.

ORGANISM(S): Mus musculus

SUBMITTER: Joshua Mendell

PROVIDER: E-GEOD-62831 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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.

2014-10-30 | GSE62831 | GEO

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

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

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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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