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MiR-200c induction in BT549 TNBC cells

ABSTRACT: We performed microarray analysis on BT549 cells that express miR-200c in a doxycycline (dox)-inducible manner from the miR-200c-TripZ system.

ORGANISM(S): Homo sapiens

PROVIDER: GSE108271 | GEO | 2017/12/20

SECONDARY ACCESSION(S): PRJNA423021

REPOSITORIES: GEO

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miR-200c induction in BT549 TNBC cells

Project description:miR-200c induction in BT549 TNBC cells

| PRJNA423021 | ENA

miR-200c induction in Met-1 mammary carcionma cells

Project description:We performed RNA-seqeuncing analysis on mouse Met-1 cells that express miR-200c in a doxycycline (DOX)-inducible manner from the miR-200c-TripZ system.

2020-05-28 | GSE151320 | GEO

Expression data from differentiating ES cells expressing miR-200c and miR-141

2011-09-22 | GSE24289 | GEO

Expression data from differentiating ES cells expressing miR-200c and miR-141

Project description:ES cells express the miR-200 family which becomes down-regulated during the course of differentiation in serum. We generated an ES cell line which expresses miR-200c and miR-141 upon addition of doxycycline. Microarrays were used to gain a global picture of differentiation when miR-200c and miR-141 expression were maintained throughout differentiation through the addition of doxycycline. A2.miR200c ES cells, which express miR-200c/miR-141 upon addition of doxycycline, were differentiated as embryoid bodies in six petri dishes. Half of the samples were treated with doxycycline on days 2 and 4 of differentiation, and RNA was collected from all samples on days 3, 4, and 5.

2011-09-21 | E-GEOD-24289 | biostudies-arrayexpress

Effect of miR-200c-3p overexpression on primary human macrophages

Project description:Macrophages constitute a major part of the tumor-infiltrating immune cells and within the tumor microenvironment acquire an alternatively activated, tumor-supporting phenotype. Factors released by tumor cells are crucial for the recruitment of tumor-associated macrophages. In the present project, we aimed to understand the role of miR-200c in the interplay between tumor cells and macrophages. To this end, we employed a coculture system of MCF7 breast tumor cells and primary human macrophages and observed a substantial transfer of miR-200c from apoptotic tumor cells to macrophages, which required intact CD36 receptor in macrophages. We further comprehensively determined miR-200c targets in macrophages by mRNA-sequencing and found numerous migration-associated mRNAs to be downregulated by miR-200c. Consequently, miR-200c attenuated macrophage infiltration into 3-dimensional tumor spheroids. The miR-200c-mediated reduction of infiltration further correlated well with a miR-200c migration signature comprised of four miR-200c-repressed targets (PPM1F, RAB11FIB2, RDX, MSN).

2022-03-30 | GSE195587 | GEO

TALEN-based knockout of mir-141 and mir-200c in SK-BR-3 cells

Project description:We used transcription activator-like effector nucleases (TALENs) to generate knockout cells for two related microRNAs (miRNAs), mir-141 and mir-200c, which belong to the deeply conserved mir-200 family. By carrying out deep sequencing, we identified the target genes of each miRNA. Interestingly, miR-141 and miR-200c, despite their overall similarity, suppressed largely non-overlapping groups of targets. Analysis of global mRNA level change in mir-141 and mir-200c knockout compared to wild type cells

2013-09-27 | E-GEOD-51217 | biostudies-arrayexpress

Restoring miR-200c to aggressive endometrial cancer cell line

Project description:Using a mimic miR-200c was restored to an aggressive, Type 2 endometrial cancer cell line, Hec50 We sought to identify genes regulated by miR-200c in an aggressive cancer.

2010-11-17 | E-GEOD-25332 | biostudies-arrayexpress

The Pitx2:miR-200c/141:noggin pathway regulates BMP signaling and ameloblast differentiation

Project description:The mouse incisor is a remarkable tooth that grows throughout the animal’s lifetime. This continuous renewal is fueled by epithelial stem cells that give rise to ameloblasts, which generate enamel, and little is known about the function of specific miRNAs in this process. Here we describe the role of a novel Pitx2:miR-200c/141:Noggin regulatory pathway in dental epithelial cell differentiation. miR-200c repressed noggin, an antagonist of Bmp signaling. Pitx2 expression caused an up-regulation of miR-200c and chromatin immunoprecipitation (ChIP) assays revealed endogenous Pitx2 binding to the miR-200c/141 promoter. A positive feedback loop was discovered between miR-200c and Bmp signaling. miR-200c/141 induced expression of E-cadherin and the dental epithelial cell differentiation marker, amelogenin. In addition, miR-203 expression was activated by endogenous Pitx2 and targeted the Bmp antagonist Bmper to further regulate Bmp signaling. miR-200c/141 knockout mice showed defects in enamel formation with decreased E-cadherin and amelogenin expression and increased noggin expression. Our in vivo and in vitro studies reveal a multistep transcriptional program involving the Pitx2:miR-200c/141:Noggin regulatory pathway that is important in epithelial cell differentiation and tooth development.

2013-07-09 | GSE48583 | GEO

TALEN-based knockout of mir-141 and mir-200c in SK-BR-3 cells

2013-09-27 | GSE51217 | GEO

lncRNA/mRNA expression profiling of miR-200c-overexpressing MDA-MB-231 cells

Project description:MiR-200c is a well-studied miRNA that is involved in stemness, the epithelial-mesenchymal transition, chemoresistance, radioresistance, and invasion/metastasis of various cancer cells. To obtain an overview of the lncRNA/mRNA regulated by miR-200c signaling in breast-cancer cell lines, we performed global lncRNA/mRNA-expression profiling on MDA-MB-231-pGIPZ and MDA-MB-231-miR-200c cells.

2018-08-28 | GSE119090 | GEO

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