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MicroRNA-200c/141 confines ERα activity and expression pattern by targeting Ccnd1

ABSTRACT: MicroRNA-200c/141 confines ERα activity and expression pattern by targeting Ccnd1

PROVIDER: PRJNA727189 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14418058.fastq.gz	Fastqsanger.gz
	SRR14418059.fastq.gz	Fastqsanger.gz
	SRR14418060_1.fastq.gz	Fastqsanger.gz
	SRR14418060_2.fastq.gz	Fastqsanger.gz
	SRR14418061_1.fastq.gz	Fastqsanger.gz

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MicroRNA-200c/141 confines ERα activity and expression pattern by targeting Ccnd1 [bulk RNA-seq]

Project description:ERα is one of the most important transcription factors and therapeutic targets in breast cancer. The patterns of ERα expression in normal breast tissue and cancerous lesions are strikingly different. What drives the change of ERα pattern during lesions formation remains unclear. Here, we describe a novel regulatory mechanism through which miR-200c/141 regulates the level as well as the distribution of ERα in the mammary gland. miR-200c/141 is specifically expressed in luminal cells. Luminal-deletion of miR-200c/141 (miR-cKO) leads to a drastic expansion of ERα+ cell proportion. Single cell RNAseq reveals that miR-cKO generates aberrant luminal subpopulations with increased proliferative and anti-apoptotic features. In vivo lineage tracing of ER- luminal cells demonstrates that miR-200c/141 deletion can convert ER- cells into ER+ cells, which contribute partly to the increase of ERα+ luminal cells. Mechanistic study identifies Ccnd1 as a novel target of miR-200c/141 . Upon miR-200c/141deletion, elevated Ccnd1 level corroborates ERα transcriptional activation, leads to enhanced ERα signaling activity, consequently increased transcription of ERα coding gene Esr1 through self-activation at promoter E1. Our findings reveal a new miR-200c/141-Ccnd1-ERα axis, and provide new molecular insights into how miR-200c/141-Ccnd1 enforces the lineage barrier between ER- and ER+ luminal cells, and what drives the change of ERα expression pattern.

2021-05-05 | GSE173815 | GEO

MicroRNA-200c/141 confines ERα activity and expression pattern by targeting Ccnd1 [single-cell RNA-seq]

2021-05-05 | GSE173816 | GEO

MicroRNA-200c/141 confines ERα activity and expression pattern by targeting Ccnd1 [bulk RNA-seq]

Project description:MicroRNA-200c/141 confines ERα activity and expression pattern by targeting Ccnd1 [bulk RNA-seq]

| PRJNA727194 | ENA

MicroRNA-200c/141 confines ERα activity and expression pattern by targeting Ccnd1 [single-cell RNA-seq]

Project description:MicroRNA-200c/141 confines ERα activity and expression pattern by targeting Ccnd1 [single-cell RNA-seq]

| PRJNA727195 | ENA

RNA sequencing of RipmiR-141~200c and RipmiR-141~200c Zeb1200M islets

Project description:We performed RNA sequencing of islets of Langerhans isolated from RipmiR-141~200c and RipmiR-141~200c Zeb1200M mice to determine the transcriptomic effects of mutating miR-200 binding sites in the endogenous Zeb1 3'UTR of mice in which miR-141~200c is overexpressed under the rat insulin promoter (RIP).

2022-04-30 | E-MTAB-10537 | biostudies-arrayexpress

RNA sequencing of RipmiR-141~200c and RipmiR-141~200c Zeb1200M islets

Project description:RNA sequencing of RipmiR-141~200c and RipmiR-141~200c Zeb1200M islets

| PRJEB45958 | ENA

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

MicroRNA-200c/141 confines ERα activity and expression pattern by targeting Ccnd1

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-05-05 | GSE173817 | 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.

2011-09-22 | GSE24289 | 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

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