Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The long non-coding RNA Falcor regulates Foxa2 expression to maintain lung epithelial homeostasis and promote regeneration

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

ORGANISM(S): Mus musculus

PROVIDER: GSE126818 | GEO | 2022/01/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

The long noncoding RNA Falcor regulates Foxa2 expression to maintain lung epithelial homeostasis and promote regeneration.

Project description:Transcription factors (TFs) are dosage-sensitive master regulators of gene expression, with haploinsufficiency frequently leading to life-threatening disease. Numerous mechanisms have evolved to tightly regulate the expression and activity of TFs at the transcriptional, translational, and posttranslational levels. A subset of long noncoding RNAs (lncRNAs) is spatially correlated with transcription factors in the genome, but the regulatory relationship between these lncRNAs and their neighboring TFs is unclear. We identified a regulatory feedback loop between the TF Foxa2 and a downstream lncRNA, Falcor (Foxa2-adjacent long noncoding RNA). Foxa2 directly represses Falcor expression by binding to its promoter, while Falcor functions in cis to positively regulate the expression of Foxa2. In the lung, loss of Falcor is sufficient to lead to chronic inflammatory changes and defective repair after airway epithelial injury. Moreover, disruption of the Falcor-Foxa2 regulatory feedback loop leads to altered cell adhesion and migration, in turn resulting in chronic peribronchial airway inflammation and goblet cell metaplasia. These data reveal that the lncRNA Falcor functions within a regulatory feedback loop to fine-tune the expression of Foxa2, maintain airway epithelial homeostasis, and promote regeneration.

| S-EPMC6546060 | biostudies-literature

The long non-coding RNA Falcor regulates Foxa2 expression to maintain lung epithelial homeostasis and promote regeneration (array)

Project description:One month following airway injury with naphthalene (275mg/kg IP x1 in corn oil), total RNA was isolated from one lobe of the right lung (whole lung) from either Falcor-/- (null) or injured wild-type control mice.

2022-01-31 | GSE126816 | GEO

The long non-coding RNA Falcor regulates Foxa2 expression to maintain lung epithelial homeostasis and promote regeneration (RNA-Seq)

Project description:EpCAM+ lung epithelial cells were isolated by magnetic bead sorting from either wild-type animals 10-12 weeks of age, or with the genotypes Falcor-/-, Foxa2+/-, or Double-Het (Falcor+/-;Foxa2+/-) animals

2022-01-31 | GSE126817 | GEO

The long non-coding RNA Falcor regulates Foxa2 expression to maintain lung epithelial homeostasis and promote regeneration

Project description:The long non-coding RNA Falcor regulates Foxa2 expression to maintain lung epithelial homeostasis and promote regeneration

| PRJNA523391 | ENA

The long non-coding RNA Falcor regulates Foxa2 expression to maintain lung epithelial homeostasis and promote regeneration (array)

Project description:The long non-coding RNA Falcor regulates Foxa2 expression to maintain lung epithelial homeostasis and promote regeneration (array)

| PRJNA523389 | ENA

The long non-coding RNA Falcor regulates Foxa2 expression to maintain lung epithelial homeostasis and promote regeneration (RNA-Seq)

Project description:The long non-coding RNA Falcor regulates Foxa2 expression to maintain lung epithelial homeostasis and promote regeneration (RNA-Seq)

| PRJNA523394 | ENA

Long non-coding RNA LncCplx2 regulates glucose homeostasis and pancreatic β cell function.

Project description:ObjectiveNumerous studies have highlighted the role of clock genes in diabetes disease and pancreatic β cell functions. However, whether rhythmic long non-coding RNAs involve in this process is unknown.MethodsRNA-seq and 3' rapid amplification of cDNA ends (RACE)-PCR were used to identify the rat LncCplx2 in pancreatic β cells. The subcellular analysis with qRT-PCR and RNA-Scope were used to assess the localization of LncCplx2. The effects of LncCplx2 overexpression or knockout (KO) on the regulation of pancreatic β cell functions were assessed in vitro and in vivo. RNA-seq, immunoblotting (IB), Immunoprecipitation (IP), RNA pull-down, and chromatin immunoprecipitation (ChIP)-PCR assays were employed to explore the regulatory mechanisms through LncRNA-protein interaction. Metabolism cage was used to measure the circadian behaviors.ResultsWe first demonstrate that LncCplx2 is a conserved nuclear long non-coding RNA and enriched in pancreatic islets, which is driven by core clock transcription factor BMAL1. LncCplx2 is downregulated in the diabetic islets and repressed by high glucose, which regulates the insulin secretion in vitro and ex vivo. Furthermore, LncCplx2 KO mice exhibit diabetic phenotypes, such as high blood glucose and impaired glucose tolerance. Notably, LncCplx2 deficiency has significant effects on circadian behavior, including prolonged period duration, decreased locomotor activity, and reduced metabolic rates. Mechanistically, LncCplx2 recruits EZH2, a core subunit of polycomb repression complex 2 (PRC2), to the promoter of target genes, thereby silencing circadian gene expression, which leads to phase shifts and amplitude changes in insulin secretion and cell cycle genes.ConclusionsOur results propose LncCplx2 as an unanticipated transcriptional regulator in a circadian system and suggest a more integral mechanism for the coordination of circadian rhythms and glucose homeostasis.

| S-EPMC10832480 | biostudies-literature

Hypoxia-induced long non-coding RNA DARS-AS1 regulates RBM39 stability to promote myeloma malignancy.

Project description:Multiple myeloma is a malignant plasma-cell disease, which is highly dependent on the hypoxic bone marrow microenvironment. However, the underlying mechanisms of hypoxia contributing to myeloma genesis are not fully understood. Here, we show that long non-coding RNA DARS-AS1 in myeloma is directly upregulated by hypoxia inducible factor (HIF)-1. Importantly, DARS-AS1 is required for the survival and tumorigenesis of myeloma cells both in vitro and in vivo DARS-AS1 exerts its function by binding RNA-binding motif protein 39 (RBM39), which impedes the interaction between RBM39 and its E3 ubiquitin ligase RNF147, and prevents RBM39 from degradation. The overexpression of RBM39 observed in myeloma cells is associated with poor prognosis. Furthermore, knockdown of DARS-AS1 inhibits the mammalian target of rapamycin signaling pathway, an effect that is reversed by RBM39 overexpression. We reveal that a novel HIF-1/DARS-AS1/RBM39 pathway is implicated in the pathogenesis of myeloma. Targeting DARS-AS1/RBM39 may, therefore, represent a novel strategy to combat myeloma.

| S-EPMC7271587 | biostudies-literature

Up-regulation of long non-coding RNA XLOC_010235 regulates epithelial-to-mesenchymal transition to promote metastasis by associating with Snail1 in gastric cancer.

Project description:We previously performed long non-coding RNA (lncRNA) expression microarray analyses to identify novel indicators for gastric cancer (GC) metastasis and prognosis in which we identified lncRNA XLOC_010235 (XLOC) as a candidate RNA. However, XLOC_010235 molecular mechanism of action remains unclear. Gain and loss of function approaches were used to investigate the biological role of XLOC in vitro. The effects of XLOC on cell viability were assessed by CCK-8 proliferation assays. Real-time PCR, western-blot and immunofluorescence were used to evaluate the mRNA and protein expression of Snail and multiple EMT related molecules. The positive XLOC/Snail1 interaction was identified and verified by immunohistochemistry assay and bivariate correlation analysis. Ectopic expression of XLOC facilitate cell viability, migration and invasion, leading to the acceleration of metastasis, while depletion of XLOC expression hindered cell migration and invasion. Moreover, over-expression of XLOC was found to play a important role in epithelial-to-mesenchymal transition (EMT) through the regulation of E-cadherin, N-cadherin and Vimentin expression, in which transcriptional factor Snail1 was involved. These results advance our understanding of the role of lncRNA XLOC_010235 as a active regulator of EMT by associating with Snail1, which may help in the development of new therapeutics.

| S-EPMC5446413 | biostudies-literature

Exosomes from high glucose-treated macrophages promote epithelial-mesenchymal transition of renal tubular epithelial cells via long non-coding RNAs.

Project description:BackgroundMacrophages contribute to epithelial-mesenchymal transition (EMT) in diabetic nephropathy (DN). Exosomal long non-coding RNAs (lncRNAs) derived from macrophages play a major role in transmitting biological information, whereas related studies on DN are rare. Here we investigated the effects of exosomal lncRNAs from high glucose-treated macrophages on EMT.MethodsHigh glucose-treated macrophage exosomes (HG-exos) were extracted by coprecipitation and stabilized. Then, mouse renal tubular epithelial cells were treated with HG-exos for 24 h. Expression of E-cadherin, α-smooth muscle actin (α-SMA), and fibronectin was detected by western blotting, qPCR, and immunofluorescence. High-throughput sequencing was then applied to analyze the bioinformatics of HG-exos.ResultsHG-exos inhibited the proliferation of tubular epithelial cells. Additionally, HG-exos markedly upregulated α-SMA and fibronectin expression and downregulated E-cadherin expression in tubular epithelial cells, indicating EMT induction. A total of 378 differentially expressed lncRNAs and 674 differentially expressed mRNAs were identified by high-throughput sequencing of HG-exos. Bioinformatics analysis and subsequent qPCR validation suggested 27 lncRNAs were enriched in the EMT-related MAPK pathway. Among them, ENSMUST00000181751.1, XR_001778608.1, and XR_880236.2 showed high homology with humans.ConclusionExosomes from macrophages induce EMT in DN and lncRNAs in exosomes enriched in the MAPK signaling pathway may be the possible mechanism.

| S-EPMC9887774 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data