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5-Fluorouracil Treatment Represses Pseudouridine-Containing miRNA Export into Extracellular Vesicles

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE255877 | GEO | 2024/09/18

REPOSITORIES: GEO

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5-Fluorouracil Treatment Represses Pseudouridine-Containing miRNA Export into Extracellular Vesicles (smallRNA seq)

Project description:5-Fluorouracil (5-FU) has been used for chemotherapy for colorectal and other cancers for over 50 years. The prevailing view of its mechanism of action is inhibition of thymidine synthase leading to defects in DNA replication and repair. However, 5-FU is also incorporated into RNA causing defects in RNA metabolism, inhibition of pseudouridine modification, and altered ribosome function. We examined the impact of 5-FU on the expression and export of small RNAs into small extracellular vesicles (sEVs) and regulation of post-transcriptional small RNA modifications (PTxMs). EVs are secreted by all cells and contain a variety of proteins and RNAs that can function in cell-cell communication. PTxMs on cellular and extracellular small RNAs provide yet another layer of gene regulation. We found that treatment of colorectal cancer (CRC) cells with 5-FU represses sEV export of miRNA and snRNA-derived RNAs, but promotes export of snoRNA-derived RNAs. Strikingly, 5-FU treatment significantly decreased the levels of pseudouridine on both cellular and sEV small RNA profiles. In contrast, 5-FU exposure led to increased levels of cellular small RNAs containing a variety of methyl-modified bases. Our results suggest that 5-FU exposure leads to altered expression, base modification, and mislocalization of sEV small RNAs.

2024-09-18 | GSE255876 | GEO

5-Fluorouracil Treatment Represses Pseudouridine-Containing miRNA Export into Extracellular Vesicles (RNA-seq)

2024-09-18 | GSE255875 | GEO

5-Fluorouracil Treatment Represses Pseudouridine-Containing miRNA Export into Extracellular Vesicles

Project description:5-Fluorouracil Treatment Represses Pseudouridine-Containing miRNA Export into Extracellular Vesicles

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5-Fluorouracil Treatment Represses Pseudouridine-Containing miRNA Export into Extracellular Vesicles (RNA-seq)

Project description:5-Fluorouracil Treatment Represses Pseudouridine-Containing miRNA Export into Extracellular Vesicles (RNA-seq)

| PRJNA1077087 | ENA

5-Fluorouracil Treatment Represses Pseudouridine-Containing miRNA Export into Extracellular Vesicles (smallRNA seq)

Project description:5-Fluorouracil Treatment Represses Pseudouridine-Containing miRNA Export into Extracellular Vesicles (smallRNA seq)

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Glioma-derived miRNA-containing extracellular vesicles induce angiogenesis by reprogramming brain endothelial cells

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

2019-12-20 | GSE138115 | GEO

Glioma-Derived miRNA-Containing Extracellular Vesicles Induce Angiogenesis by Reprogramming Brain Endothelial Cells.

Project description:Glioblastoma (GBM) is characterized by aberrant vascularization and a complex tumor microenvironment. The failure of anti-angiogenic therapies suggests pathways of GBM neovascularization, possibly attributable to glioblastoma stem cells (GSCs) and their interplay with the tumor microenvironment. It has been established that GSC-derived extracellular vesicles (GSC-EVs) and their cargoes are proangiogenic in vitro. To further elucidate EV-mediated mechanisms of neovascularization in vitro, we perform RNA-seq and DNA methylation profiling of human brain endothelial cells exposed to GSC-EVs. To correlate these results to tumors in vivo, we perform histoepigenetic analysis of GBM molecular profiles in the TCGA collection. Remarkably, GSC-EVs and normal vascular growth factors stimulate highly distinct gene regulatory responses that converge on angiogenesis. The response to GSC-EVs shows a footprint of post-transcriptional gene silencing by EV-derived miRNAs. Our results provide insights into targetable angiogenesis pathways in GBM and miRNA candidates for liquid biopsy biomarkers.

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miRNA expression of extracellular vesicles

Project description:To further investigate the molecular mechanisms by which EVs mediated the abnormal localization of tight junction proteins and adherence junction protein, we performed miRNA microarray analysis of extracellular vesicles isolated from breast cancer cells. miRNA expression in extracellular vesicles was collected from MDA-MB-231-D3H1, MDA-MB-231-D3H2LN, BMD2a and BMD2b breast cancer cell lines.

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Osteoblasts secrete miRNA-containing extracellular vesicles that enhance expansion of human umbilical cord blood cells.

Project description:Osteolineage cells represent one of the critical bone marrow niche components that support maintenance of hematopoietic stem and progenitor cells (HSPCs). Recent studies demonstrate that extracellular vesicles (EVs) regulate stem cell development via horizontal transfer of bioactive cargo, including microRNAs (miRNAs). Using next-generation sequencing we show that human osteoblast-derived EVs contain highly abundant miRNAs specifically enriched in EVs, including critical regulators of hematopoietic proliferation (e.g., miR-29a). EV treatment of human umbilical cord blood-derived CD34(+) HSPCs alters the expression of candidate miRNA targets, such as HBP1, BCL2 and PTEN. Furthermore, EVs enhance proliferation of CD34(+) cells and their immature subsets in growth factor-driven ex vivo expansion cultures. Importantly, EV-expanded cells retain their differentiation capacity in vitro and successfully engraft in vivo. These discoveries reveal a novel osteoblast-derived EV-mediated mechanism for regulation of HSPC proliferation and warrant consideration of EV-miRNAs for the development of expansion strategies to treat hematological disorders.

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Adipose Tissue Macrophages Modulate Obesity-Associated β Cell Adaptations through Secreted miRNA-Containing Extracellular Vesicles.

Project description:Obesity induces an adaptive expansion of β cell mass and insulin secretion abnormality. Expansion of adipose tissue macrophages (ATMs) is a hallmark of obesity. Here, we assessed a novel role of ATMs in mediating obesity-induced β cell adaptation through the release of miRNA-containing extracellular vesicles (EVs). In both in vivo and in vitro experiments, we show that ATM EVs derived from obese mice notably suppress insulin secretion and enhance β cell proliferation. We also observed similar phenotypes from human islets after obese ATM EV treatment. Importantly, depletion of miRNAs blunts the effects of obese ATM EVs, as evidenced by minimal effects of obese DicerKO ATM EVs on β cell responses. miR-155 is a highly enriched miRNA within obese ATM EVs and miR-155 overexpressed in β cells impairs insulin secretion and enhances β cell proliferation. In contrast, knockout of miR-155 attenuates the regulation of obese ATM EVs on β cell responses. We further demonstrate that the miR-155-Mafb axis plays a critical role in controlling β cell responses. These studies show a novel mechanism by which ATM-derived EVs act as endocrine vehicles delivering miRNAs and subsequently mediating obesity-associated β cell adaptation and dysfunction.

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