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MiRNA-1229-5p promotes the migration and invasion of endometrial cells by regulating STMN1/EMT in ovarian endometriosis

ABSTRACT: miRNA-1229-5p promotes the migration and invasion of endometrial cells by regulating STMN1/EMT in ovarian endometriosis

PROVIDER: PRJNA1110983 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29006257_1.fastq.gz	Fastqsanger.gz
	SRR29006257_2.fastq.gz	Fastqsanger.gz
	SRR29006258_1.fastq.gz	Fastqsanger.gz
	SRR29006258_2.fastq.gz	Fastqsanger.gz
	SRR29006259_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

miRNA-1229-5p promotes the migration and invasion of endometrial cells by regulating STMN1/EMT in ovarian endometriosis

Project description:Emerging evidence suggests that aberrantly expressed microRNAs (miRNAs) participate in endometriosis pathogenesis. Our previous miRNA microarray analysis revealed dysregulated expression of miR-1229-5p in eutopic endometrial stromal cells (ESCs) from ovarian endometriosis patients compared with healthy controls. However, the role and mechanism of miR-1229-5p in EMs remain unclear.

2025-05-10 | GSE267283 | GEO

miR-193b-5p and miR-374b-5p are aberrantly expressed in endometriosis and suppress endometrial cell migration in vitro

Project description:Endometriosis is a highly prevalent gynecological disease affecting 10% of women of reproductive age worldwide. miRNAs may play a role in endometriosis, though their exact function remains unclear. Here, we identified differentially expressed miRNAs in endometriosis and studied their functional role in the disease. (2) Methods: Endometrial tissue was collected from women with endometriosis (n=15) and non-endometriosis controls (n=17). Dysregulated miRNAs were identified through small RNA-sequencing, and their biological significance was explored by target gene prediction and pathway analysis. Selected miRNAs were examined in paired ectopic endometriomas and eutopic endometrium (n=10) using qRT-PCR. Their roles in cell migration and proliferation were further examined in vitro using functional assays. To identify potential target genes, we performed mRNA sequencing on transfected cells and the endometrioma cohort. (3) Results: We identified 14 dysregulated miRNAs in the eutopic endometrium of women with endometriosis compared to endometrial tissue from women without endometriosis. Pathway analysis indicated enrichment in cell migration and proliferation associated pathways. Further ex-vivo studies of miR-193b-5p and miR-374b-5p showed that both miRNAs were up-regulated in endometriomas. Overexpression of these two miRNAs in vitro inhibited cell migration and mRNA sequencing revealed several migration-related genes that are targeted by these miRNAs. (4) Conclusions: Our study identified two key endometrial miRNAs that may be involved in the pathogenesis of endometriosis by regulating cell migration.

2024-11-08 | GSE279835 | GEO

miR-193b-5p and miR-374b-5p Are Aberrantly Expressed in Endometriosis and Suppress Endometrial Cell Migration In Vitro

Project description:(1) Background: Endometriosis is a prevalent gynecological disease affecting 1 out of 10 women of reproductive age. MicroRNAs (miRNAs) may play a role in endometriosis, though their exact function is unclear. In this study we aimed to identify differentially expressed miRNAs in endometriosis and study their functional role in the disease. (2) Methods: Endometrial tissue was collected from patients with endometriosis (n=15) and healthy controls (n=17). Dysregulated miR-NAs were identified through small RNA-sequencing, and their function were explored by target gene prediction and pathway analysis. Selected miRNAs were validated in a cohort of paired ec-topic endometriomas and eutopic endometrium (n=10) using RT-qPCR. Their role in cell migration and proliferation were further examined in vitro using functional assays. To identify potential target genes, we performed mRNA sequencing of the miRNA-transfected cells and endometrioma cohort. (3) Results: We identified 14 dysregulated miRNAs in eutopic endometrium from women with en-dometriosis. Pathway analysis indicated enrichment in cell migration and proliferation pathways. miR-193b-5p and miR-374b-5p, selected for validation, were up-regulated in endometrioma. Over-expression of these two miRNAs in-vitro inhibited cell migration and mRNA sequencing further revealed that several genes related to cell migration are targeted by these miRNAs. (4) Conclusions: Our study identified two key endometrial miRNAs that may be involved in the pathogenesis of endometriosis by regulating cell migration.

2024-10-29 | GSE275002 | GEO

miR-1199-5p and Zeb1: a novel double-negative feedback coordinating EMT and tumour cell invasion (mRNA-seq)

Project description:We investigated the effect of miR-1199-5p, miR-200b-3p and miR-429-3p on gene expression profiles during TGFbeta-induced EMT in normal murine mammary gland cells by using the mRNA-sequencing. Our analysis demonstrates that miR-1199-5p and both miR-200 family members share only 6 target genes, indicating that besides regulating Zeb1 expression they exert distinct functions during EMT.

2017-11-09 | GSE86024 | GEO

miR-205-5p Inhibits Human Endometriosis Progression by Targeting ANGTP2 in Endometrial Stromal Cells

Project description:the newly identified miR-205-5p-ANGPT2-AKT/ERK axis illustrates the molecular mechanism of endometriosis progression and may represent a novel diagnostic biomarker and therapeutic target for disease treatment.

2018-12-19 | GSE124010 | GEO

miR-193b-5p and miR-374b-5p Are Aberrantly Expressed in Endometriosis and Suppress Endometrial Cell Migration In Vitro

Project description:miR-193b-5p and miR-374b-5p Are Aberrantly Expressed in Endometriosis and Suppress Endometrial Cell Migration In Vitro

| PRJNA1148930 | ENA

miR-193b-5p and miR-374b-5p are aberrantly expressed in endometriosis and suppress endometrial cell migration in vitro

Project description:miR-193b-5p and miR-374b-5p are aberrantly expressed in endometriosis and suppress endometrial cell migration in vitro

| PRJNA1174758 | ENA

Oviductal extracellular vesicles from women with endometriosis impair embryo development

Project description:Objective To investigate the influence that oviductal extracellular vesicles from patients with endometriosis exert on early embryo development. Design In vitro experimental study Setting University-affiliated hospital. Patient(s) Women with and without endometriosis who underwent hysterectomy (n = 15 in total). Intervention(s) None. Main Outcome Measure(s) Oviductal extracellular vesicles from patients with endometriosis (oEV-EMT) or without endometriosis (oEV-ctrl) were isolated and co-cultured with two-cell murine embryos for 75 hours. Blastocyst rates were recorded. RNA sequencing was used to identified the differentially expressed genes in blastocysts cultured either with oEV-EMT or with oEV-ctrl. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were performed to identify potential biological processes in embryos that oEV-EMT affect. The functions of oEV on early embryo development were determined by reactive oxygen species (ROS) levels, mitochondrial membrane potentials, total cell numbers and apoptotic cell proportions. Result(s) Extracellular vesicles were successfully isolated from human Fallopian tubal fluid and their characterizations were described. The blastocyst rates were significantly decreased in the oEV-EMT group. RNA sequencing revealed that oxidative phosphorylation was down-regulated in blastocysts cultured with oEV-EMT. Analysis of oxidative stress and apoptosis at the blastocysts stage showed that embryos cultured with oEV-EMT had increased ROS level, decreased mitochondrial membrane potentials, and increased apoptotic index. Total cell numbers were not influenced. Conclusion(s) Oviductal extracellular vesicles from patients with endometriosis exert a negative influence on early embryo development.

2023-06-02 | GSE225323 | GEO

Peritoneal endometriosis

Project description:We performed gene expression analysis human peritoneal endometriosis lesions, eutopic endometrium from endometriosis patients and peritoneum form endometriosis patients.The goal of the study was to analyse gene expression differences between peritoneal endometriosis lesion and eutopic endometrium and peritoneal endometriosis lesion and peritoneum.

2012-12-06 | E-MTAB-694 | biostudies-arrayexpress

EGF Induces Migration Independent of EMT or Invasion in A549 Lung Adenocarcinoma Cells

Project description:Tumors and tumor surrounding tissues produce multiple growth factors that influence tumor cell behavior via different signal transduction pathways. Growth factors like transforming growth factor beta (TGFβ) and epidermal growth factor (EGF) were shown to induce proliferation, migration and invasion in different cell models. Both factors are frequently overexpressed in cancer and will often act in combination. Although both factors are being used as rational targets in clinical oncology, similarities and differences of their contributions to cancer cell migration and invasion are not fully understood. Here we compared the impact of TGFβ, EGF and the combination of both factors on A549 cells. Both factors stimulated A549 migration to a similar extent but with a different kinetic and the combination had an additive effect. While EGF-induced migration depended on activation of the mitogen-activated protein kinase (MAPK) pathway, this pathway was dispensable for TGFβ-induced migration despite a strong activation by TGFβ. Proteome analysis revealed an overlap in expression patterns of migration-related proteins and associated gene ontology (GO) terms by TGFβ and EGF but only TGFβ induced the expression of epithelial to mesenchymal transition (EMT)-related proteins like matrix metalloproteinase 2 (MMP2). EGF in contrast, made no major contribution to EMT marker expression on either the protein or the transcript level. In line with these expression patterns, EGF was unable to increase invasion of A549 cells on its own and failed to enhance TGFβ-induced invasion. Overall, these data suggest that TGFβ and EGF may partly compensate each other for stimulation of cell migration but abrogation of TGFβ signaling may be more suitable for antagonizing invasion.

2021-04-08 | PXD023024 | Pride

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