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Intercellular transfer of miR-200c-3p impairs the angiogenic capacity of cardiac endothelial cells

ABSTRACT: Intercellular transfer of miR-200c-3p impairs the angiogenic capacity of cardiac endothelial cells

PROVIDER: PRJNA792146 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17328463.fastq.gz	Fastqsanger.gz
	SRR17328464.fastq.gz	Fastqsanger.gz
	SRR17328465.fastq.gz	Fastqsanger.gz
	SRR17328466.fastq.gz	Fastqsanger.gz
	SRR17328468.fastq.gz	Fastqsanger.gz

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Intercellular transfer of miR-200c-3p impairs the angiogenic capacity of cardiac endothelial cells

Project description:We identify miR-200c-3p as a microRNA to be enriched in cardiomyocyte (CM)-derived EVs under conditions of hypertrophic stress. This miRNA is transferred from CMs to cardiac endothelial cells (ECs) where it will impair endothelial cell function.RNA sequencing was performed to identify the mechanisms and genes that are under direct or indirect control of miR-200c and that could explain the phenotypes observed.

2022-01-31 | GSE192586 | GEO

Transcriptomic analysis of hepatocellular carcinoma cell lines HepG2 treated with Sorafenib and transfected with miR-200c-3p inhibitor, and miR-222-5p and miR-512-3p mimics

Project description:Hepatocellular carcinoma (HCC) is one of the most common causes of death worldwide and the fourth most prevalent type of cancer. Whereas curative treatments such as liver transplantation, ablation or surgery are optimal for early stages, only paliative treatments are given to intermediate and advanced stages of the disease. Despite the introduction of immune regulators as first-line treatments for advanced stages, Sorafenib is still the standard of care in the clinical practice. In cell lysates, anti-tumoral properties of Sorafenib were related to upregulation of miR-200c-3p (anti-tumoral miRNA) at 6 hours of treatment and downregulation of miR-222-5p and miR-512-3p (pro-tumoral miRNAs) at 24 hours. We have identified these miRNA biomarkers of Sorafenib treatment response in plasma of patients with advanced HCC treated with Sorafenib. In particular, miR-200c-3p has been related to increased survival benefit whereas miR-222-5p and miR-512-3p have been related to worse prognosis. Our study has sequenced HepG2 cells treated with Sorafenib and miR-200c-3p inhibitor, and transfected with miR-222-5p and miR-512-3p mimics to unravel the molecular pathways governing Sorafenib response

2022-04-28 | GSE201695 | GEO

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

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

| PRJNA801287 | ENA

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

Glomerular endothelial derived vesicles mediate podocyte dysfunction via extracellular transfer of miRNA-200c-3p

Project description:Glomerular endothelial derived vesicles mediate podocyte dysfunction via extracellular transfer of miRNA-200c-3p

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miR-200c-3p, miR-222-5p and miR-512-3p are outcome circulating biomarkers in patients with hepatocarcinoma under Sorafenib treatment

Project description:miR-200c-3p, miR-222-5p and miR-512-3p are outcome circulating biomarkers in patients with hepatocarcinoma under Sorafenib treatment

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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

miR-200c induction in BT549 TNBC cells

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

2017-12-20 | GSE108271 | GEO

Cancer cell-endothelial intercellular transfer alters the endogenous miRNA profile and phenotype of recipient endothelial cells

Project description:Metastasis is a major cause of mortality, and remains a final frontier in the search for a cure for cancer. While there has been much research on the ‘seed’ (metastatic tumor cells) and the ‘soil’ (colonized host tissue), interactions between metastatic cancer cells and stromal endothelial cells, which occur at multiple stages during metastasis, are less well understood. Here we report a dynamic regulation of the endothelium by cancer cells through the formation of nanoscale intercellular membrane bridges, which act as physical conduits for intercellular communication in vitro and in vivo, including horizontal transfer of microRNAs (miRNA). The communication between the tumor cell and the endothelium upregulates markers associated with pathological endothelium, which is reversed by pharmacological inhibition of these nanoscale conduits. These results lead us to define the notion of “metastatic hijack”: cancer cell-induced transformation of healthy endothelium into pathological endothelium via horizontal communication through the nanoscale conduits. Pharmacological perturbation of these nanoscale membrane bridges decreases metastatic foci in syngeneic- and human xenograft-breast cancer models. Targeting the formation of these nanoscale membrane bridges may potentially emerge as a new therapeutic opportunity in the management of metastatic cancer. A miRNA microarray was used to evaluate the transport of endogenous microRNAs. The intercellular transfer-ve and intercellular transfer+ve samples were sorted from the same endothelial cell population with the only difference being the occurrence of intercellular transport. The heat map shows potential miRNA candidates for exogenous transfer on two independent biological replicates. These miRNA candidates were significantly up-regulated in the cells receiving transfer of intercellular contents. HUVECs that were not exposed to cancer cells were used as a baseline control.

2015-09-04 | E-GEOD-72679 | biostudies-arrayexpress

NCoR1 limits angiogenic capacity by altering Notch signaling

Project description:Corepressors negatively regulate gene expression by chromatin compaction. Targeted regulation of gene expression could provide a means to control endothelial cell phenotype. We hypothesize that by targeting corepressor proteins, endothelial angiogenic function can be improved. To study this, the expression and function of nuclear corepressors in human umbilical vein endothelial cells (HUVEC) and in murine organ culture was studied. RNA-seq revealed that nuclear receptor corepressor 1 (NCoR1), Silencing Mediator of Retinoid and Thyroid hormone receptors (SMRT) and repressor element-1 silencing transcription factor (REST) are the highest expressed corepressors in HUVECs. Knockout and knockdown strategies demonstrated that the depletion of NCoR1 increased the angiogenic capacity of endothelial cells, whereas depletion of SMRT or REST did not. Interestingly, the effect was VEGF signaling independent. NCoR1 depletion significantly upregulated angiogenesis-associated genes, especially tip cell genes, including ESM1, DLL4 and NOTCH4, as observed by RNA- and ATAC-seq. Confrontation assays comparing cells with and without NCoR1-deficiency revealed that loss of NCoR1 promotes a tip-cell position during spheroid sprouting. Moreover, a proximity ligation assay identified NCoR1 as a direct binding partner of the Notch-signaling-related transcription factor RBPJk. Luciferase assays showed that siRNA-mediated knockdown of NCoR1 promotes RBPJk activity. Furthermore, NCoR1 downregulation prompts upregulation of several elements in the Notch signaling cascade. Downregulation of NOTCH4, but not NOTCH1, prevented the positive effect of NCoR1 knockdown on spheroid outgrowth. Collectively, these data indicate that decreasing NCOR1 expression is an attractive approach to promote angiogenic function. This SuperSeries is composed of the SubSeries listed below.

2024-02-12 | GSE237654 | GEO

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