LINC01638 promotes epithelial-to-mesenchymal transition in endometriosis epithelial cells by upregulating RHOB via HDAC1 suppression
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ABSTRACT:
PROVIDER: PRJNA1186174 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31350813_1.fastq.gz | Fastqsanger.gz | |||
| SRR31350813_2.fastq.gz | Fastqsanger.gz | |||
| SRR31350814_1.fastq.gz | Fastqsanger.gz | |||
| SRR31350814_2.fastq.gz | Fastqsanger.gz | |||
| SRR31350815_1.fastq.gz | Fastqsanger.gz |
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Project description:Endometriosis is a common disease in women characterized by the growth of endometrial-like lesions at ectopic sites, associated with chronic pelvic pain and infertility. LINC01638 is a long non-coding RNA (lncRNA) that in several cancers has been implicated in the regulation of proliferation and epithelial-to-mesenchymal transition (EMT). Given that these processes are also important in endometriosis, we investigated the role of LINC01638 in this disease. We found that LINC01638 is upregulated in the epithelial layer of endometriosis lesions, and that knockdown of the gene in 12Z epithelial endometriosis cell line led to reduced proliferation, adhesion, migration and invasion. The reduction in proliferation was associated with increased p21 and p27 expression and G1 phase arrest of 12Z cells, showing that LINC01638 acts as an important epigenetic regulator of endometriosis epithelial cells cell cycle progression. Further, transcriptome analysis of LINC01638 control and knockdown cells revealed that a number of transcription factors associated with EMT are downregulated in the knockdown, including FOXC2, SNAI2, TWIST1 and ZEB1, along with the mesenchymal marker VIM. These genetic and phenotypic changes in 12Z knockdown cells were accompanied by a significant reduction in expression of cytoskeleton regulatory gene RHOB and an upregulation of HDAC1 expression. Chromatin immunoprecipitation analysis and HDAC1 inhibitory treatment in LINC01638 control and knockdown cells indicated that LINC01638 regulates RHOB expression via HDAC1 mediated regulation of its promoter acetylation. In vivo, RHOB is upregulated in the epithelial layer of endometriosis lesions compared to control and endometriosis patient eutopic endometrium, supporting a role in the disease. Together these results indicate that LINC01638 is an epigenetic regulator of pathogenesis of endometriosis promoting proliferation and EMT of endometriosis lesions.
2025-02-16 | GSE281916 | GEO
Project description:Purpose: RhoB regulates cell functions, such as vesicular transport, apoptosis, autophagy, DNA repair, angiogenesis, proliferation, migration and invasion. We investigated whether RhoB is involved in the pathogenesis of ulcerative colitis (UC).We performed RNA sequencing analysis in intestinal epithelial cells (IECs) from RhoB-deficient mice and WT mice to study the molecular mechanisms through which RhoB regulates goblet cell numbers and epithelial regeneration and confirmed findings in colonic organoids from RhoB-deficient mice and WT mice and siRhoB transfected SW480 cells.
2022-09-27 | GSE170994 | GEO
Project description:We have performed quantitative proteomic TandemMassTag to investigate proteomic changes after deletion of epigenetic eraser genes Hdac1 and Hdac2 in intestinal epithelial cells. Both HDAC1 and HDAC2 are epigenetic erasers that drive specific and redundant gene expression patterns, in part by removing acetyl groups on histones. Deletion of these Hdac in intestinal epithelial cell (IEC) in vivo alters intestinal homeostasis, dependent on the Hdac deleted and the level of expression of both. To determine the specific IEC function of HDAC1 and HDAC2, we have performed transcriptomic and quantitative proteomic approaches on IEC deficient in Hdac1 and Hdac2. We have defined changes in both mRNA and protein expression patterns affecting IEC differentiation. We have identified IEC Hdac1- and Hdac2-dependent common as well as specific pathways and biological processes. These findings uncover unrecognized similarities and differences between Hdac1 and Hdac2 in IEC.
2021-09-09 | PXD022558 | Pride
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:Endometriosis is a common gynecological disorder characterized by ectopic growth of endometrium outside the uterus and associated with chronic pain and infertility. We investigated the role of LINC01133 in endometriosis, an lncRNA that has been implicated in several types of cancer. We found that LINC01133 is upregulated in ectopic endometriosis lesions. As expression appeared higher in the epithelial endometrial layer, we performed an siRNA knockdown of LINC01133 in an endometriosis epithelial cell line. Phenotypic assays indicated that LINC01133 may promote proliferation and suppress cellular migration, and affect the cytoskeleton and morphology of the cells. Gene ontology analysis of differentially expressed genes detected by RNA sequencing indicated that cell proliferation and migration pathways were affected in line with the observed phenotype. We validated upregulation of p21 and downregulation of cyclin at the protein level, which together with DNA FACS analysis indicated that the observed effects on cellular proliferation may be due to changes in cell cycle progression. Further, we validated upregulation of the protein kinase TESK1 at the protein level, and found a corresponding increased phosphorylation and therefore inactivation of the actin severing protein Cofilin, which may explain changes in the cytoskeleton and cellular migration. These results indicate that LINC01133 upregulation is associated with endometriosis, which may be due to its effects on genes involved in the cellular proliferation and migration pathways.
2021-08-23 | GSE174741 | GEO
Project description:RHOB, a member of the Rho GTPase family, is a target of miR-1915-3p. miR-1915-3p has been proved by us to affect the differentiation of MEPs, promoting the differentiation of megakaryocytes and inhibiting the erythroid lineage, which may lead to an increase in the number of platelets and a decrease in the number of erythrocytes. Although RHOB has been confirmed to be involved in the process of proplatelets production in mice, its role in early hematopoietic differentiation, especially its impact on the megakaryocytic and erythroid differentiation of human HSCs and MEPs, has not yet been elucidated. In this study, we confirmed that the function of the RHOB gene was opposite to miR-1915-3p by knocking down the gene in progenitor cells and inducing them into different cells. Silencing of RHOB significantly decreased the erythroid surface markers, reduced the diameter of the cell and inhibited the expression of erythroid-related genes in human cells. Furthermore, RHOB knockdown in megakaryocytic-induced cells increased the megakaryocytic surface markers, enlarged cell and nuclear volume and promoted cell polyploidy and megakaryocyte-related gene expression. The results of RNA sequencing suggest that the RHOB may play a role in differentiation by influencing the cell cycle and the cytoskeleton. Based on that, we found RHOB could affect the expression of differential CDKs and cyclins to alter the proportions of G0/1 and S phase cells and influent the expression or aggregation of β-ACTIN during erythroid or megakaryocytic differentiation. Taken together, these results suggest that RHOB plays an important role in megakaryocytic and erythroid differentiation by cell cycle and cytoskeleton regulation.
2025-04-23 | GSE282217 | GEO
Project description:RhoB null mice show decreases in pathological angiogenesis in the ischemic retina and reduces angiogenesis in response to cutaneous wounding, but enhances lymphangiogenesis following both dermal wounding and inflammatory challenge. We used microarrays to link these unique and opposing roles of RhoB in blood versus lymphatic vasculatures to RhoB/VEZF1-mediated gene regulation in primary human blood versus lymphatic endothelial cells.
2013-10-28 | GSE51754 | GEO
Project description:RhoB null mice show decreases in pathological angiogenesis in the ischemic retina and reduces angiogenesis in response to cutaneous wounding, but enhances lymphangiogenesis following both dermal wounding and inflammatory challenge. We used microarrays to link these unique and opposing roles of RhoB in blood versus lymphatic vasculatures to RhoB/VEZF1-mediated gene regulation in primary human blood versus lymphatic endothelial cells. Pure populations of human primary BVECs and LVECs silenced for RhoB or VEZF1 were used for RNA extraction and hybridization on Affymetrix microarrays. We extracted these cells from human male foreskins from at least four individuals and purified them using Dynabeads associated with vascular markers (CD31 and Podoplanin).
2013-10-28 | E-GEOD-51754 | biostudies-arrayexpress
Project description:We profiled transcriptomes of >370,000 individual cells from endometriomas (n=8), endometriosis (n=28), eutopic endometrium (n=10), unaffected ovary (n=4) and endometriosis-free peritoneum (n=4) to create a cellular atlas of endometrial-type epithelial cells, stromal cells, and microenvironmental cell populations across tissue sites.
2022-10-11 | GSE213216 | GEO
Project description:This project aims at comparing endometrium from women with and without endometriosis during the secretory phase of menstrual cycle. The present results constitute a first step towards identifying potential diagnosis biomarkers and may provide a better understanding of endometriosis especially the etiology of the disease.
2022-04-01 | PXD012981 | Pride