FOXQ1 is a critical regulator of the mammary epithelial to mesenchymal transcription program
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA593005 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10574354.fastq.gz | Fastqsanger.gz | |||
| SRR10574355.fastq.gz | Fastqsanger.gz | |||
| SRR10574356.fastq.gz | Fastqsanger.gz | |||
| SRR10574357.fastq.gz | Fastqsanger.gz | |||
| SRR10574358.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 16 |
Similar Datasets
Project description:Purpose: The goals of this study were to uncover the epithelial to mesenchymal transcription program under direct regulation by FOXQ1 and to characterize the KMT2/MLL histone methyl transferase complex as a transcriptional co-activator for the FOXQ1 EMT program.
2020-12-01 | GSE141293 | GEO
Project description:The Forkhead family of transcription factors comprises numerous members and is implicated in various cellular functions, including cell growth, apoptosis, migration and differentiation.In this study we identified the Forkhead factor FoxQ1 as increased in expression during TGF-beta1 induced changes in epithelial differentiation, suggesting functional roles of FoxQ1 for epithelial plasticity.The repression of FoxQ1 in mammary epithelial cells led to a change in cell morphology characterized by an increase in cell size, pronounced cell-cell contacts and an increased expression of several junction proteins (e.g. E-cadherin). In addition, FoxQ1 knock-down cells revealed rearrangements in the actin-cytoskeleton and slowed down cell cycle G1-phase progression.Furthermore, repression of FoxQ1 enhanced the migratory capacity of coherent mammary epithelial cells.Gene expression profiling of NM18 cells indicated that FoxQ1 is a relevant downstream mediator of TGF-beta1 induced gene expression changes. This included the differential expression of transcription factors involved in epithelial plasticity, e.g. Ets-1, Zeb1 and Zeb2.In summary, this study has elucidated the functional impact of FoxQ1 on epithelial differentiation
2010-09-01 | GSE23833 | GEO
Project description:The forkhead box transcription factor FOXQ1 is aberrantly induced in various cancers, and contributes to tumour growth and metastasis. It has been suggested that the oncogenic potential of FOXQ1 may be explained by its activation of the Wnt/β-catenin signalling pathway. However, the mode of action of FOXQ1 in the Wnt pathway remains to be resolved. Here we report that FOXQ1 is bimodal transcriptional regulator of Wnt target gene expression in normal and cancer cells. Using co-immunoprecipitation, proximity proteomics, and reporter assays, we show that FOXQ1 partly engages the Wnt transcriptional complex to promote gene expression via TCF/LEF transcription factors.
2022-10-05 | PXD035624 | Pride
Project description:The Forkhead family of transcription factors comprises numerous members and is implicated in various cellular functions, including cell growth, apoptosis, migration and differentiation.In this study we identified the Forkhead factor FoxQ1 as increased in expression during TGF-beta1 induced changes in epithelial differentiation, suggesting functional roles of FoxQ1 for epithelial plasticity.The repression of FoxQ1 in mammary epithelial cells led to a change in cell morphology characterized by an increase in cell size, pronounced cell-cell contacts and an increased expression of several junction proteins (e.g. E-cadherin). In addition, FoxQ1 knock-down cells revealed rearrangements in the actin-cytoskeleton and slowed down cell cycle G1-phase progression.Furthermore, repression of FoxQ1 enhanced the migratory capacity of coherent mammary epithelial cells.Gene expression profiling of NM18 cells indicated that FoxQ1 is a relevant downstream mediator of TGF-beta1 induced gene expression changes. This included the differential expression of transcription factors involved in epithelial plasticity, e.g. Ets-1, Zeb1 and Zeb2.In summary, this study has elucidated the functional impact of FoxQ1 on epithelial differentiation Cells treated with 200µM 4sU for 2h, biological replicate 1:2h_co._total1, Cells treated with 200µM 4sU for 2h, biological replicate 2:2h_co._total2, Cells treated with 200µM 4sU for 2h, biological replicate 3 :2h_co._total3, Cells treated with 200µM 4sU for 2h and enriched for 4sU labelled RNA, biological replicate 1: 2h_co._enriched1, Cells treated with 200µM 4sU for 2h and enriched for 4sU labelled RNA, biological replicate 2: 2h_co._enriched2, Cells treated with 200µM 4sU for 2h and enriched for 4sU labelled RNA, biological replicate 3:2h_co._enriched3, Cells treated with 5 ng/ml TGF-b1 and 200µM 4sU for 2h, biological replicate 1:2h_TGFbeta_total1, Cells treated with 5 ng/ml TGF-b1 and 200µM 4sU for 2h, biological replicate 2:2h_TGFbeta_total2, Cells treated with 5 ng/ml TGF-b1 and 200µM 4sU for 2h, biological replicate 3:2h_TGFbeta_total3, Cells treated with 5 ng/ml TGF-b1 and 200µM 4sU for 2h and enriched for 4sU labelled RNA, biological replicate 1:2h_TGFbeta_enriched1, Cells treated with 5 ng/ml TGF-b1 and 200µM 4sU for 2h and enriched for 4sU labelled RNA, biological replicate 2:2h_TGFbeta_enriched2, Cells treated with 5 ng/ml TGF-b1 and 200µM 4sU for 2h and enriched for 4sU labelled RNA, biological replicate 3:2h_TGFbeta_enriched3, FoxQ1 dataset Cells transfected with 25nm scrambled siRNA for 48hrs, biological replicate 1:ns-siRNA 48hrs 1, Cells transfected with 25nm scrambled siRNA for 48hrs, biological replicate 2:ns-siRNA 48hrs 2, Cells transfected with 25nm scrambled siRNA for 48hrs, biological replicate 3:ns-siRNA 48hrs 3, Cells transfected with 25nm scrambled siRNA for 48hrs and treated with TGF-b1 for 40hrs biological replicate 1:ns-siRNA 48hrs TGF-b1 40hrs 1, Cells transfected with 25nm scrambled siRNA for 48hrs and treated with TGF-b1 for 40hrs biological replicate 2:ns-siRNA 48hrs TGF-b1 40hrs 2, Cells transfected with 25nm scrambled siRNA for 48hrs and treated with TGF-b1 for 40hrs biological replicate 3:ns-siRNA 48hrs TGF-b1 40hrs 3, Cells transfected with 25nm FoxQ1 siRNA for 48hrs and treated with TGF-b1 for 40hrs biological replicate 1:FoxQ1 siRNA 48hrs TGF-b1 40hrs 1, Cells transfected with 25nm FoxQ1 siRNA for 48hrs and treated with TGF-b1 for 40hrs biological replicate 2:FoxQ1 siRNA 48hrs TGF-b1 40hrs 2 Cells transfected with 25nm FoxQ1 siRNA for 48hrs and treated with TGF-b1 for 40hrs biological replicate 3:FoxQ1 siRNA 48hrs TGF-b1 40hrs 3
2010-09-01 | E-GEOD-23833 | biostudies-arrayexpress
Project description:FOXQ1 is a putative oncogene in several types of carcinomas and, in colorectal cancers, is one of the most highly upregulated genes. FOXQ1 has been previously identified as a candidate Wnt pathway activator in CRC cells. However, it is still unclear how the crosstalk between FOXQ1 and Wnt signalling influence the global behaviour of colorectal cancer cells. Here, we performed bulk RNA sequencing of FOXQ1 or vector transfected HCT116 cells with or without Wnt3a treatment. Each condition was performed in biological triplicates.
2022-09-23 | E-MTAB-12062 | biostudies-arrayexpress
Project description:Kaiso, a critical regulator of spermatogenesis
| PRJNA436947 | ENA
Project description:We report the genome wide RNA sequencing for high-throughput profiling of FOXQ1 target genes in melanoma and carcinoma cells. We generated melanoma (SK-Mel-147) and ovarian carcinoma cells (SCOV3) ectopically expressing FOXQ1. We find that FOXQ1 differentially regulates the expression of several genes in melanoma cells as compared to carcinoma cells. Specifically, FOXQ1 induces the expression of several genes in ovarian carcinoma cells SCOV3 and suppresses the expression of the same genes in melanom cells. We show that this differentialy regulation of the same target gene depends upon the nuclear levels of beta-catenin. High levels of active nuclear beta-catenin promote FOXQ1 mediated transcriptional activation of genes whereas low levels contribute to TLE/Groucho- mediated repression. This study provides a framework for understanding the lineage specific pattern of transcriptional regulation by FOXQ1 and its contextual determinants.
2017-08-25 | GSE103071 | GEO
Project description:To explore FOXQ1’s transcriptional role, we utilized an HA-tagged FOXQ1 plasmid for CUTTag enabling high-resolution mapping of FOXQ1 binding sites on the genome.
2024-07-16 | GSE271829 | GEO
Project description:Transcription factor Foxq1 controls mucin gene expression and granule content in mouse stomach surface mucous cells ; Background and Aims: The gastric mucosa provides a stringent epithelial barrier and produces acid and enzymes that initiate digestion. In this regenerating tissue, progenitors differentiate continually into 4 principal specialized cell types, yet underlying mechanisms of differentiation are poorly understood. We identified stomach-restricted expression of the forkhead transcription factor FOXQ1. Methods: We used a combination of genetic, histochemical, ultrastructural and molecular analysis to study gastric cell lineages with respect to FOXQ1. Results: Within the developing and adult gastrointestinal tract, Foxq1 mRNA is restricted to the stomach, expressed prominently in foveolar (pit) cells, the abundant mucin-producing cells that line the mucosal surface, and required for their complete differentiation. Mice carrying Foxq1 coding mutations show virtual absence of mRNA and protein for the backbone of the predominant stomach mucin, MUC5AC. These observations correspond to a paucity of foveolar-cell secretory vesicles and notable loss of stomach but not intestinal mucus. Transcriptional profiling identified a surprisingly restricted set of genes with altered expression in Foxq1 mutant stomachs. MUC5AC is a highly tissue-restricted product that similarly depends on FOXQ1 in its other major site of expression, conjunctival goblet cells. Conclusions: Taken together, these observations imply that promotion of gastric MUC5AC synthesis is a primary, cell-autonomous function of FOXQ1. This study is the first to implicate a transcription factor in terminal differentiation of foveolar cells and begins to define the requirements to assemble highly specialized organelles and cells in the gastric mucosa. DOI: 10.1053/j.gastro.2008.04.019 Experiment Overall Design: RNA from stomach antrum from 2 of each Satin, Beige, and BL6 mice were compared using microarray analysis.
2008-06-16 | E-GEOD-8943 | biostudies-arrayexpress
Project description:Ovarian cancer has increasingly been linked with lipid metabolism disturbances, while the association between circulating low-density lipoprotein (LDL) levels and ovarian cancer remains controversial. our study found that high serum LDL promoted migration, invasion, epithelial-mesenchymal transition (EMT) and stemness of ovarian cancer cells. Through high throughput sequencing, we found LDL enhanced the expression of genes related to EMT and stemness pathways in ovarian cancer cells. Besides, the effect might be facilitated by upregulating the critical transcription factor FOXQ1. Overall, our study uncovers a mechanism underlying metastasis in ovarian cancer cells, and suggests potential clinical strategies controlling serum LDL levels or targeting FOXQ1 to prevent ovarian cancer progression.
2025-07-05 | GSE301160 | GEO