MiRNA-1229-5p promotes the migration and invasion of endometrial cells by regulating STMN1/EMT in ovarian endometriosis
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE267283 | GEO | 2025/05/10
REPOSITORIES: GEO
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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
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
Project description:Background. Endometriosis (EMS) is a chronic, gynecological condition affecting 6-10% of reproductive-age women. While these lesions are benign, ovarian EMS present cancer-like features, and can progress to endometriosis-correlated ovarian cancer (ECOC) through a multistep process. Given the regulatory role of miRNAs in gene expression and biological pathways, we aimed to identify miRNAs associated with the malignant transformation of ovarian EMS, which could serve as a potential diagnostic tool for the early identification of such patients. Methods. Global miRNA profiling was performed in patients with benign ovarian EMS (EMS-b) and patients with ECOC. Differential expression analysis (DEA) of miRNAs between EMS-b, EMS tissues from patients with ECOC (EMS-k) and ECOC tissues was performed. Receiver Operating Characteristic (ROC) curves were built to evaluate the binary classification performance of significant miRNAs. Results. Comparison between EMS-b and EMS-k revealed 13 significantly deregulated miRNAs. Furthermore, when comparing ECOC and EMS-b we observed significant deregulation of 181 miRNAs. ROC analysis revealed a panel of seven upregulated miRNAs with accuracies above 0.7 in identifying EMS-k and EMS-b. Notably, four miRNAs (hsa-miR-200a-3p, hsa-miR-141-3p, hsa-miR-183-5p, hsa-miR-10a-5p) were consistently upregulated in both EMS-k and ECOC tissues. Conclusions. Our study identified a panel of miRNA biomarkers that may serve as potential candidates for the early detection of ECOC in patients previously diagnosed with ovarian EMS.
2025-04-16 | GSE292134 | GEO
Project description:Background Reduced endometrial receptivity is a major factor for impaired fertility in endometriosis (EMS). Endometrial deposition of collagen I proteins may account for poor endometrial receptivity in endometriosis. Methods We investigated the expression of collagen I expression in endometrium of endometriosis patients and in constructed EMS mice model. Effect of collagen I on ESCs was evaluated. Co-culture of exosomes with ESCs was conducted to evaluate the uptake of exosomes by different endometrial cell lines and the effect on decidualization of eutopic ESCs and embryo implantation. MiRNA expression profiles were compared between ectopic ESC derived exosomes and eutopic ESC derived exosomes. Luciferase reporter and its mutant plasmids were applied to confirm the direct target of miR-25-3p. Findings Here we found endometrial collagen I deposition with impaired decidualization in endometriosis patients and EMS mice model. Treatment of collagen I with ESCs contributed to impaired decidualization and inhibited BLS expansion in vitro. Endometriotic stromal cell-derived exosomes were detected in eutopic endometrium and the ectopic endometrial stromal cell derived exosomes were more taken-up by the same cell line in eutopic endometrium. Treatment of endometriotic stromal cell-derived exosomes increased the expression of endometrial collagen I in vitro and in vivo, while inhibited BLS expansion. Exosomal miR-25-3p was significantly increased in endometriotic stromal cell-derived exosomes compared with control group, and PTEN is a certain target of miR-25-3p. The promotion of endometrial miR-25-3p significantly increased collagen I expression in vitro through the PTEN/Akt pathway. Interpretation These results suggested that endometriotic stromal cell-derived exosomal miR-25-3p played key role in inducing endometrial collagen I deposition to impair embryo expansion in endometriosis via PTEN/Akt pathway. Funding National Nature Science Foundation of China (82271702), National Natural Science Foundation of China (81771537). Keywords: endometriosis; exosome; collagen I; miRNA; collagen deposition
2025-01-28 | GSE222432 | GEO
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
Project description:Accumulating evidence suggests that microRNAs play definite roles in the pathogenesis of endometriosis. The objective of the study was to determine the role of miR-100-5p, one of the upregulated microRNA in endometriotic cyst stromal cells, in the pathogenesis of endometriosis. Downstream targets of miR-100-5p were identified by compulsory expression of miR-100-5p in normal eutopic endometrial stromal cells (NESCs), a global mRNA microarray technique, and pathways analysis.Compulsory expression of miR-100-5p in NESCs directed the induction of cell motility through SWItch/sucrose non-fermentable (SWI/SNF)-related matrix-associated actin-dependent regulator of chromatin subfamily D member 1 (SMARCD1) supression and matrix metallopeptidase 1 (MMP1) activation.
2020-04-22 | GSE139954 | GEO
Project description:miRNA-1229-5p promotes the migration and invasion of endometrial cells by regulating STMN1/EMT in ovarian endometriosis
| PRJNA1110983 | ENA
Project description:Endometriosis (EMs) is a common infertility-related disease in women of reproductive age. Impaired endometrial decidualization is one of the most important factors contributing to the embryo implantation failure EMs patients. However, the exact mechanism remains unclear. Previous studies have shown collagen I deposition in the eutopic endometrium of EMs patients, which may lead to impaired endometrial decidualization. The level of collagen I in eutopic endometrium of EMs was analyzed. We performed a proteomic analysis of ectopic endometrial stromal cell-derived extracellular vesicles (EMs-EVs) and extracellular vesicles derived from endometrial stromal cells in the endometrium of control patients (CTL-EVs). An endometrial transcriptional profiles of EMs patients and normal controls in the mid-secretory phase of menstrual cycle was compared. Endometrial stromal cells (ESCs) were stimulated with chloroquine or rapamycin to evaluate the association between autophagy and collagen I. The expression of PKM2 in EMs-EVs and serum extracellular vesicles from EMs patients were examined by western blotting. PKM2 was overexpressed or knockdown in ESCs to investigate the level of autophagy and collagen I. ESCs were treated with ectopic ESC-derived extracellular vesicles with highly expressed PKM2 protein, and the potential molecular mechanisms were further confirmed through western blotting and immunohistochemical analysis. We found that endometrial collagen I expression during the mid-secretory phase was increased in the EMs group. We demonstrated that autophagy is defective in eutopic endometrial stromal cells (ESCs) of EMs patients. In ESCs, pharmacological inhibition of autophagy by chloroquine (CQ) promoted collagen I deposition. Ectopic endometrial stromal cell-derived extracellular vesicles (EMs-EVs) inhibited autophagy of ESCs and promoted collagen I deposition in vivo and in vitro. Mechanistically, EMs-EVs encapsulating PKM2 impair eutopic endometrial autophagy via Akt/mTOR signaling pathway. Together, we demonstrated that EMs-EVs encapsulating PKM2 impaired endometrial autophagy inducing collagen I deposition in EMs, which provided a potential target for therapeutic implications.
2025-02-22 | GSE278827 | GEO
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
Project description:The pathogenesis of endometriosis may result from aberrant angiogenesis that occurs in eutopic endometrium with retrograde menstruation. The difference in gene expression profile between human endometrial endothelial cells (HEECs) from eutopic endometria of patients with and without endometriosis would be determinant that affects the occurrence of endometriosis. To explore this kind of difference, we performed in vitro culture and identified their endothelial origin, as well as observed growth features of HEECs from the two different origins. Finally we identified the difference in gene expression profile when combined suppression subtractive hybridization(SSH) with genechip and confirmed the results by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The HEECs derived from endometriosis exhibited potent survival ability in vitro compared to that from non-endometriosis. We found that gremlin and fibronectin genes were up-regulated in HEECs derived from eutopic endometrium of patients with endometriosis when compared with that from patients without endometriosis. Our study implies that enhanced angiogenic capacity of eutopic HEECs may be an independent determinant in endometriotic aberrant angiogenesis in addition to the interaction of exfoliated endometrium and peritoneal environment elements such as activated macrophages and soluble cytokines. Experiment Overall Design: We analyzed 5 arrays for HEECs derived from eutopic endometrium of patients with endometriosis and 5 arrays for HEECs derived from that of patients without endometriosis
2008-06-15 | E-GEOD-7846 | biostudies-arrayexpress