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Mouse ureter: wild type vs miR-143/145 knock out

ABSTRACT: mRNA profiling of mouse ureters comparing wild-type ureter vs. ureters from mice having whole body deletion of miR-143 and miR-145 which results in abnormal ureter peristalsis and hydronephrosis We used microarrays to detail the global program of gene expression in wild-type and miR-143/145-deficient ureters which revealed dysregulation of genes linked to smooth muscle morphology and function.

ORGANISM(S): Mus musculus

PROVIDER: GSE58274 | GEO | 2014/10/08

SECONDARY ACCESSION(S): PRJNA251871

REPOSITORIES: GEO

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Mouse ureter: wild type vs miR-143/145 knock out

Project description:mRNA profiling of mouse ureters comparing wild-type ureter vs. ureters from mice having whole body deletion of miR-143 and miR-145 which results in abnormal ureter peristalsis and hydronephrosis We used microarrays to detail the global program of gene expression in wild-type and miR-143/145-deficient ureters which revealed dysregulation of genes linked to smooth muscle morphology and function. Two condition experiment: wild type vs miR-143/145 KO; biological replicates: individual mice - 2 wild type, 2 mutant. One replicate per array.

2014-10-08 | E-GEOD-58274 | biostudies-arrayexpress

The mir-143-145 cluster plays a pro-tumorigenic role in lung adenocarcinoma by promoting neoangiogenesis

Project description:A growing body of literature has proposed cell-autonomous tumor suppressor functions for the mir-143~145 cluster in a variety of human cancers, including lung adenocarcinoma, and has reported therapeutic benefits of delivering mir-143 and mir- 145 to tumors. In contrast to these studies, we found that depletion or forced expression of mir-143 and mir-145 in an autochthonous mouse model of lung adenocarcinoma did not affect tumor development. Surprisingly, we observed that loss of mir-143~145 from the tumor microenvironment significantly reduced tumor burden, indicating a non-cell- autonomous role for these miRNAs in promoting tumorigenesis. By examining the expression patterns of different cell populations isolated in vivo from tumor-bearing lungs using an integrated computational approach, we identified a role for mir-145 in stimulating the proliferation of endothelial cells by downregulating an inhibitory kinase, Camk1d, which prevents mitotic entry. As a consequence, tumors in mir-143~145- deficient animals exhibited diminished hallmarks of neo-angiogenesis, increased apoptosis and their expansion appeared limited by the tumor’s ability to co-opt the alveolar vasculature. These findings show that expression of the mir-143~145 cluster in the tumor stroma promotes rather than suppresses tumorigenesis and cautions against the use of these miRNAs as agents in cancer therapeutics.

2016-05-21 | GSE71877 | GEO

Analysis of miR-143/145 wild-type and null mouse intestinal myofibroblasts before and after LPS stimulation

Project description:In a series of mouse genetic studies, we concluded that miR-143/145 expression in intestinal subepithelial myofibroblasts (ISEMFs) promotes epithelial regeneration after DSS-mediated injury in the colon. This experiment aims to identify miR-143/145 target genes that are involved in this function. We generated primary ISEMFs from wildtype and miR-143/145 null mouse colons and analyzed their gene expression profile. We further subjected ISEMFs to LPS treatment, in order to measure gene expression changes that are only revealed after inflammatory stress.

2014-05-22 | GSE55651 | GEO

rs41291957 alters secondary RNA structure of the human pri-miR-143/145

Project description:Purpose: To evaluate whether the single nucleotide polimorphsim rs41291957, located in the pri-miR-143/145, influences the primary RNA secondary structure. Methods: In vitro transcription and folding for the pri-miR-143/145 carrying the WT allele (G) or the mutated one (A) was carried out. The RNAs were then subjected to RNAseI treatement for 30 minutes and RNA seq performed on the digested nucleic acids. Results: Using an optimized data analysis workflow for small RNAs, we mapped the sequence reads on the human pri-miR-143/145 carrying the G- or A-allele. We observed an increase of small reads (<60bps) for the A-allele and a different profile of read enrichement between the digested G- and A-allele RNA, indicating the difference in secondary structure.

2021-07-15 | GSE180017 | GEO

Analysis of miR-143/145 wild-type and null mouse intestinal myofibroblasts before and after LPS stimulation

2014-05-22 | E-GEOD-55651 | biostudies-arrayexpress

Mice heart: wild-type mice vs. alpha MHC/mir-143/145 transgenic mice

Project description:Transcriptional profilings of the mouse heart obtained from control (wild-type) and alpha MHC/mir-143/145 transgenic mouse line 9 and 19.

2019-04-01 | GSE112355 | GEO

RNA-Seq analysis of human M238P melanoma cells transduced with a lentivirus expressing the miR-143/145 cluster or a control lentivirus

Project description:To assess the transcriptomic response associated with upregulation of the miR-143/-145 cluster, BRAFV600E mutant human melanoma cells M238P cells were transduced for stable expression of miR-143/145 cluster or with a control vector. Forty-eight hours after transduction, cells were treated with 1 μg/mL of puromycin for one week. RNA samples were then harvested. Two independent experiments were carried out.

2021-12-29 | GSE171881 | GEO

Impact of miR-143-3p and miR-145-5p overexpression on human M238P melanoma cells

Project description:To identify putative novel specific targets of miR-143-3p and miR-145-5p, we overexpressed these miRNAs in BRAFV600E mutant human M238P melanoma cells using synthetic mimics or a synthetic “negative” control mimic (miR-Neg). RNA samples were harvested 48 hours post-transfection and 2 independent experiments were carried out.

2021-12-29 | GSE171880 | GEO

Blockade of the pro-fibrotic reaction mediated by the miR-143/-145 cluster enhances the responses to targeted therapy in melanoma

Project description:Lineage dedifferentiation towards a mesenchymal-like state displaying myofibroblast and fibrotic features is a common mechanism of adaptive and resistance to targeted therapy in melanoma. Here we show that the anti-fibrotic drug Nintedanib is active to normalize the fibrous ECM network, enhance the efficacy of MAPK-targeted therapy and delay tumor relapse in a pre-clinical model of melanoma. Acquisition of this resistant phenotype and its reversion by Nintedanib pointed to miR-143/-145 pro-fibrotic cluster as a driver of this mesenchymal-like phenotype. Upregulation of the miR-143/-145 cluster under BRAFi/MAPKi therapy was observed in melanoma cells in vitro and in vivo and was associated with an invasive/undifferentiated profile. The 2 mature miRNAs generated from this cluster, miR-143-3p and miR-145-5p collaborated to mediate transition towards a drug resistant undifferentiated mesenchymal-like state by targeting Fascin actin-bundling protein 1 (FSCN1), modulating the dynamic crosstalk between the actin cytoskeleton and the ECM through the regulation of focal adhesion dynamics and mechanotransduction pathways. Our study brings insights into a novel miRNA-mediated regulatory network that contributes to non-genetic adaptive drug resistance and provides proof-of-principle that preventing MAPKi-induced pro-fibrotic stromal response is a viable therapeutic opportunity for patients on targeted therapy.

2021-12-29 | GSE171883 | GEO

microRNA-143/145 loss induces Ras-signaling and cooperates with Pten-deficiency to promote basal-like breast cancer [CGH]

Project description:The tumor suppressor PTEN is frequently inactivated in breast and other cancers; yet, germ-line mutations in this gene induce non-malignant hamartomas, indicating dependency on additional cooperating events. Here we show that most tumors derived from conditional deletion of mouse Pten in mammary epithelium are highly differentiated and lack transplantable tumor initiating cells (TICs) capable of seeding new tumors following orthotopic injection of FACS-sorted or tumorsphere cells. A rare group of poorly differentiated tumors did harbour transplantable TICs. These transplantable tumors exhibited distinct molecular classification, signaling pathways, chromosomal aberrations and mutational landscape, as well as reduced expression of microRNA-143/145. Stable knockdown of miR-143/145 conferred tumorigenic potential upon poorly transplantable Pten-deficient tumor cells through a mechanism involving induction of RAS signaling, leading to increased sensitivity to MEK inhibition. In humans, miR145-deficiency significantly correlated with elevated RAS pathway activity in basal-like breast cancer, and patients with combined PTEN/miR-145 loss or PTEN-loss/RAS pathway activation exhibited poor clinical outcome. These results underscore a selective pressure for combined PTEN loss together with miR-145 loss or high RAS-pathway activity in aggressive forms of breast cancer, and a need to identify and prioritize these tumors for aggressive therapy. Array CGH data comparing 2 types of Pten-deficient tumors (well and poorly differentiated) with other modles of mouse mammary tumors

2017-08-18 | GSE99495 | GEO

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