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

ABSTRACT: 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

ORGANISM(S): Mus musculus

PROVIDER: GSE126817 | GEO | 2022/01/31

REPOSITORIES: GEO

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

Project description: Not available

| S-EPMC6546060 | biostudies-literature

Insm1 cooperates with Neurod1 and Foxa2 to maintain mature pancreatic β-cell function (Insm1, Neurod1 and Foxa2 ChipSeq data from pancreatic beta cell)

Project description:Genome-wide Insm1 binding sites analysis revealed an overrepresentation of sequences predicted to bind bHLH and/or forkhead factors, and further analyses demonstrated that most Insm1 sites in the genome are co-occupied by Neurod1 and Foxa2. Binding regions co-occupied by all three factors but not single Insm1 sites explained a significant fraction of gene expression changes in Insm1 mutant β-cells. Together, our data provide evidence that an Insm1, Neurod1 and Foxa2 network maintains a mature gene expression program in β-cells. 6 samples include, replicates of Insm1 and Foxa2, IgG pull down as a control

2015-03-31 | E-GEOD-54046 | biostudies-arrayexpress

Gene expression profile of Huh7 cells upon knock-down of FOXA2 or FOXA2-DS-S

Project description:We used siRNAs to knock-down the gene FOXA2 and the positionally-conserved ncRNA (pcRNA) FOXA2-DS-S is Huh7. We have shown that FOXA2 regulates its own expression by binding its promoter, but it can also affect the expression of the associated pcRNA FOXA2-DS-S. At the same time, we have shown that FOXA2-DS-S is necessary for the expression of the FOXA2 gene. These data suggest that the pcRNA acts locally, in cis, to regulate the expression of FOXA2. With this microarray experiment with aimed to explore further the genome-wide transcriptional effects of FOXA2-DS-S or FOXA2 knock-down.

2018-01-09 | E-MTAB-4517 | biostudies-arrayexpress

Insm1 cooperates with Neurod1 and Foxa2 to maintain mature pancreatic β-cell function (Insm1, Neurod1 and Foxa2 ChipSeq data from pancreatic beta cell)

2015-03-31 | GSE54046 | GEO

FOXA2 suppresses endometrial carcinogenesis and epithelial-mesenchymal transition by regulating enhancer activity

Project description:FOXA2 encodes a transcription factor mutated in 10% of endometrial cancers (ECs), with a higher mutation rate in aggressive variants. FOXA2 has essential roles in embryonic and uterine development. However, FOXA2’s role in EC is incompletely understood. Functional investigations using human and mouse EC cell lines revealed that FOXA2 controls endometrial epithelial gene expression programs regulating cell proliferation, adhesion, and endometrial-epithelial transition. In live animals, conditional inactivation of Foxa2 or Pten alone in endometrial epithelium did not result in ECs, but simultaneous inactivation of both genes resulted in lethal ECs with complete penetrance, establishing potent synergism between Foxa2 and PI3K signaling. Studies in tumor-derived cell lines and organoids highlighted additional invasion and cell growth phenotypes associated with malignant transformation and identified key mediators, including Myc and Cdh1. Transcriptome and cistrome analyses revealed that FOXA2 broadly controls gene expression programs through modification of enhancer activity in addition to regulating specific target genes, rationalizing its tumor suppressor functions. By integrating results from our cell lines, organoids, animal models, and patient data, our findings demonstrated that FOXA2 is an endometrial tumor suppressor associated with aggressive disease and with shared commonalities among its roles in endometrial function and carcinogenesis.

2022-06-14 | GSE193165 | 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

FOXA2 suppresses endometrial carcinogenesis and epithelial-mesenchymal transition through its actions as chromatin remodeler [WT67]

Project description:FOXA2 encodes a transcription factor mutated in 10% of endometrial cancers (ECs), with a higher mutation rate in aggressive variants. FOXA2 has essential roles in embryonic and uterine development. However, FOXA2’s role in EC is not understood. Functional investigations using human and mouse EC cell lines revealed that FOXA2 controls endometrial epithelial gene expression programs regulating cell proliferation, adhesion, and endometrial-epithelial transition. In live animals, conditional inactivation of Foxa2 or Pten alone in endometrial epithelium did not result in ECs, but simultaneous inactivation of both genes resulted in lethal ECs with complete penetrance, establishing potent synergism between Foxa2 and PI3K signalling. Organoids and tumor-derived cell line studies highlighted additional invasion and cell growth phenotypes associated with malignant transformation and identified key mediators including Myc and Cdh1. Transcriptome and cistrome analyses revealed that FOXA2 broadly controls gene expression programs through chromatin remodeling and modification of enhancer activity in addition to regulating specific target genes, rationalizing its tumor suppressor functions. By integrating results from our cell lines, organoids, animal models, and patient data, our findings demonstrate that FOXA2 is an endometrial tumor suppressor associated with aggressive disease and with shared commonalities among its roles in endometrial function and carcinogenesis.

2022-06-22 | GSE197210 | GEO

FOXA2 suppresses endometrial carcinogenesis and epithelial-mesenchymal transition through its actions as chromatin remodeler [WT41]

Project description:FOXA2 encodes a transcription factor mutated in 10% of endometrial cancers (ECs), with a higher mutation rate in aggressive variants. FOXA2 has essential roles in embryonic and uterine development. However, FOXA2’s role in EC is not understood. Functional investigations using human and mouse EC cell lines revealed that FOXA2 controls endometrial epithelial gene expression programs regulating cell proliferation, adhesion, and endometrial-epithelial transition. In live animals, conditional inactivation of Foxa2 or Pten alone in endometrial epithelium did not result in ECs, but simultaneous inactivation of both genes resulted in lethal ECs with complete penetrance, establishing potent synergism between Foxa2 and PI3K signalling. Organoids and tumor-derived cell line studies highlighted additional invasion and cell growth phenotypes associated with malignant transformation and identified key mediators including Myc and Cdh1. Transcriptome and cistrome analyses revealed that FOXA2 broadly controls gene expression programs through chromatin remodeling and modification of enhancer activity in addition to regulating specific target genes, rationalizing its tumor suppressor functions. By integrating results from our cell lines, organoids, animal models, and patient data, our findings demonstrate that FOXA2 is an endometrial tumor suppressor associated with aggressive disease and with shared commonalities among its roles in endometrial function and carcinogenesis.

2022-06-22 | GSE197209 | GEO

FOXA2 suppresses endometrial carcinogenesis and epithelial-mesenchymal transition through its actions as chromatin remodeler [WT106]

Project description:FOXA2 encodes a transcription factor mutated in 10% of endometrial cancers (ECs), with a higher mutation rate in aggressive variants. FOXA2 has essential roles in embryonic and uterine development. However, FOXA2’s role in EC is not understood. Functional investigations using human and mouse EC cell lines revealed that FOXA2 controls endometrial epithelial gene expression programs regulating cell proliferation, adhesion, and endometrial-epithelial transition. In live animals, conditional inactivation of Foxa2 or Pten alone in endometrial epithelium did not result in ECs, but simultaneous inactivation of both genes resulted in lethal ECs with complete penetrance, establishing potent synergism between Foxa2 and PI3K signalling. Organoids and tumor-derived cell line studies highlighted additional invasion and cell growth phenotypes associated with malignant transformation and identified key mediators including Myc and Cdh1. Transcriptome and cistrome analyses revealed that FOXA2 broadly controls gene expression programs through chromatin remodeling and modification of enhancer activity in addition to regulating specific target genes, rationalizing its tumor suppressor functions. By integrating results from our cell lines, organoids, animal models, and patient data, our findings demonstrate that FOXA2 is an endometrial tumor suppressor associated with aggressive disease and with shared commonalities among its roles in endometrial function and carcinogenesis.

2022-06-22 | GSE197208 | GEO

Human Rhinovirus Infection of the Respiratory Tract Affects Sphingolipid Synthesis

Project description:We report the application of bulk RNA sequencing to RNA extracted from lung tissue and magnetic bead isolated EpCAM+ lung epithelial cells and CD45+ lung immune cells from mice. Heterozygous serine palmitory transferase subunit 2 , Sptlc2+/- (SPT) and Sptlc2+/+ controls (WT) mice were included. Differential gene expression analysis reveals genes within the sphingolipid synthesis pathway are similarly expressed in the lung and lung epithelial cells of RV infected WT mice and SPT mice (both infected and uninfected).

2021-11-20 | GSE189056 | GEO

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