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The microRNA-200 family regulates pancreatic beta-cell survival in type 2 diabetes (Min6 cells)

ABSTRACT: The microRNAs miR-141 and -200c were co-overexpressed in the Min6 beta-cell line, which caused pro-apoptotic gene expression and subsquently apoptosis. We used Affymetrix Chip analysis to address which genes are regulated upon miR-200-overexpression to define target genes of miR-200 and pro-apoptotic genes upregulated by miR-200 to induce apoptosis.

ORGANISM(S): Mus musculus

PROVIDER: GSE58487 | GEO | 2015/05/06

SECONDARY ACCESSION(S): PRJNA252782

REPOSITORIES: GEO

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The microRNA-200 family regulates pancreatic beta-cell survival in type 2 diabetes (Min6 cells)

Project description:The microRNAs miR-141 and -200c were co-overexpressed in the Min6 beta-cell line, which caused pro-apoptotic gene expression and subsquently apoptosis. We used Affymetrix Chip analysis to address which genes are regulated upon miR-200-overexpression to define target genes of miR-200 and pro-apoptotic genes upregulated by miR-200 to induce apoptosis. Min6 cells were infected with a control Adenovirus or Adenovirus overexpression miR-141/200c. Cells were harvested with Trizol and RNA extraction was performed. RNA from n=3 wells was pooled for each condition and subjected to Affymetrix chip analysis

2015-05-06 | E-GEOD-58487 | biostudies-arrayexpress

The microRNA-200 family regulates pancreatic beta-cell survival in type 2 diabetes (islet)

Project description:Islets from control and beta-cell specific miR-141/200c overexpressing mice were extracted and Affymetrix gene expression analysis performed We used Affymetrix Chip analysis to address which genes are regulated upon miR-200-overexpression in beta-cells at the age of 6 weeks. Transgenic mice overexpressing miR-141/200c and control mice were subjected to islet extraction, RNA was extracted using Trizol method, and Affymetrix analysis was performed.

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The microRNA-200 family regulates pancreatic beta-cell survival in type 2 diabetes (islet)

2015-05-06 | GSE58488 | GEO

RNA-seq of Mus musculus beta cells to determine the role of the miR-200–Zeb1 axis in beta cell tumor development

Project description:Islet samples were sequenced to determine the effect of miR-200 KO or miR-200 site mutation in Zeb1 on tumorigenesis in RT2 mice; re-expression of individual miR-200 family members in miR-200KO cells was performed to determine the individual roles of miR-141 and miR-200c seeds

2018-11-07 | E-MTAB-6717 | biostudies-arrayexpress

Global changes in gene expression in response to miR-200 overexpression in 4TO7 cells

Project description:Transcriptional profiling of 4TO7 cells stably overexpressing miR-200s or CDH1. We observe a dramatic shift in the gene signatures when miR-200s (cluster 2; miR-200c/141, or both clusters) are overexpressed relative to controls. However, cluster 1 overexpression (miRs-200b/a/429) alone or CDH1 overexpression does not induce global changes in gene expression to levels observed for cluster 2 (miR-200c/141) or both clusters together.

2010-12-23 | GSE19631 | GEO

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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).

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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

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

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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.

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MicroRNA-200c/141 confines ERα activity and expression pattern by targeting Ccnd1 [single-cell 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 | GSE173816 | GEO

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