Analysis of transcriptome changes arising from MIR205HG modulation in prostate cells
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ABSTRACT:
PROVIDER: PRJNA407929 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Aside serving as host gene for the microRNA miR-205, MIR205HG transcribes for a nuclear chromatin-associated long noncoding RNA (lncRNA) able to restrain the differentiation of prostate basal cells, a finding that led to its reannotation as LEADR (Long Epithelial Alu-interacting Differentiation-related RNA). In our previous work (PMID: 30659180), we showed that genes that are modulated upon manipulation of MIR205HG/LEADR are characterized by the presence of an Alu sequence in their promoters. Notably, an Alu element also spans the first and second exon of MIR205HG/LEADR, thus suggesting its possible involvement in target selection and binding. Here, we performed Chromatin Isolation by RNA precipitation followed by DNA-sequencing (ChIRP-seq) to map MIR205HG/LEADR chromatin occupancy at a genome-wide level in prostate basal cells.
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Project description:This SuperSeries is composed of the SubSeries listed below.
2019-01-23 | GSE104003 | GEO
Project description:We aimed at analyzing the transcriptome changes associated with MIR205HG knock-down in RWPE-1 cells
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Project description:We aimed at analyzing the transcriptome changes associated with MIR205HG knock-down in RWPE-1 cells or overexpression in DU145 cells
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Project description:We aimed at analyzing the transcriptome changes associated with the deletion of a portion of the Alu element from MIR205HG transcript
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Project description:Genome-wide chromatin occupancy of MIR205HG/LEADR in prostate basal epithelial cells
| PRJNA832237 | ENA
Project description:Although the role of miR-205 has been widely elucidated, the function of its host gene (MIR205HG) is yet to be clarified. We have recently investigated whether this gene is a simple endorsement for miRNA production or it may act independently, demonstrating its action as nuclear long noncoding RNA able to control basal-luminal differentiation in the human prostate context, thus deserving the reannotation as LEADR, Long Epithelial Alu-interacting Differentiation-related RNA. Here, we describe the loss and gain of function approaches experimentally used to modulate LEADR expression, and the bioinformatic procedures employed to analyze microarray data in our published article "LEADeR role of miR-205 host gene as long noncoding RNA in prostate basal cell differentiation" [1]. The high reproducibility of replicates, the strong concordance with a validation technique, and the coherent behavior observed for differentially expression features, both in terms of single genes and deregulated pathways, not only support the quality of the data, but also endorse their potential reuse. Very relevant are the diverse silencing and overexpression strategies employed (all of which analyzed in multiple biologically independent replicates), which should allow other scientists to analyze our dataset for the specific purpose of their research, may it be the study of MIR205HG function as miRNA host gene, the investigation of its miRNA-independent biological role or again the dissection of Alu sequence involvement in the mechanism of action of long noncoding RNAs, which is a hot topic in the field.
| S-EPMC6992947 | biostudies-literature
Project description:Idiopathic pulmonary fibrosis (IPF) causes remodelling of distal lung, leading to respiratory failure. Pulmonary remodelling is characterised histologically not only by fibrosis but by also appearance of basal cells, yet the involvement of basal cells to IPF pathogenesis remains unclear. Here, we focus on the long non-coding RNA MIR205HG highly expressed in basal cells by single-cell RNA sequencing, to elucidate their role in IPF. Through RNA sequencing of genetic manipulations using primary cells and IPF-derived airway organoids, we uncovered MIR205HG to regulate IL33 expression. Mechanistically, the AluJb element of MIR205HG plays a key role in IL33 expression. In addition, we successfully identified a small molecule that targets this AluJb element and decreases IL33 expression. IL33 is known to induce ILC2, and MIR205HG expression positively correlated with the number of ILC2 in IPF patients. Collectively, these findings provide insights into the contributing mechanisms of basal cells to IPF and potential therapeutic targets.
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Project description:Idiopathic pulmonary fibrosis (IPF) causes remodelling of distal lung, leading to respiratory failure. Pulmonary remodelling is characterised histologically not only by fibrosis but by also appearance of basal cells, yet the involvement of basal cells to IPF pathogenesis remains unclear. Here, we focus on the long non-coding RNA MIR205HG highly expressed in basal cells by single-cell RNA sequencing, to elucidate their role in IPF. Through RNA sequencing of genetic manipulations using primary cells and IPF-derived airway organoids, we uncovered MIR205HG to regulate IL33 expression. Mechanistically, the AluJb element of MIR205HG plays a key role in IL33 expression. In addition, we successfully identified a small molecule that targets this AluJb element and decreases IL33 expression. IL33 is known to induce ILC2, and MIR205HG expression positively correlated with the number of ILC2 in IPF patients. Collectively, these findings provide insights into the contributing mechanisms of basal cells to IPF and potential therapeutic targets.
2025-03-10 | GSE275720 | GEO
Project description:Idiopathic pulmonary fibrosis (IPF) causes remodelling of distal lung, leading to respiratory failure. Pulmonary remodelling is characterised histologically not only by fibrosis but by also appearance of basal cells, yet the involvement of basal cells to IPF pathogenesis remains unclear. Here, we focus on the long non-coding RNA MIR205HG highly expressed in basal cells by single-cell RNA sequencing, to elucidate their role in IPF. Through RNA sequencing of genetic manipulations using primary cells and IPF-derived airway organoids, we uncovered MIR205HG to regulate IL33 expression. Mechanistically, the AluJb element of MIR205HG plays a key role in IL33 expression. In addition, we successfully identified a small molecule that targets this AluJb element and decreases IL33 expression. IL33 is known to induce ILC2, and MIR205HG expression positively correlated with the number of ILC2 in IPF patients. Collectively, these findings provide insights into the contributing mechanisms of basal cells to IPF and potential therapeutic targets.
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