Transcription (co)factor and miRNA regulatory landscape of EMT
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ABSTRACT:
PROVIDER: PRJNA474727 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcription (co)factor and miRNA regulatory landscape of EMT (miRNA-seq)
| PRJNA449849 | ENA
Project description:Transcription (co)factor regulatory landscape of EMT [mRNA-seq]
| PRJNA474731 | ENA
Project description:To investigate the transcriptional remodelling during EMT, we transfected normal murine mammary gland epithelial cells during a 4d TGFbeta treatment individually with siRNA against 46 transcription (co)factors or with 13 mature miRNA, all factors that blocked EMT in a phenotypic microscopy-based EMT screen upon RNAi . As a control, cells were transfected with siRNA/miRNA control followed by 4d TGFbeta treatment (mesenchymal control) or were left untreated (epithelial control). miRNA-sequencing together with mRNA-sequencing of these EMT perturbations in combination with transcription factor binding and miRNA target prediction enabled us to build an interaction map between these EMT factors.
2021-04-06 | GSE113038 | GEO
Project description:To investigate the transcriptional remodelling during EMT, we transfected normal murine mammary gland epithelial cells during a 4d TGFbeta treatment individually with siRNA against 46 transcription (co)factors or with 13 mature miRNA, all factors that blocked EMT in a phenotypic microscopy-based EMT screen upon RNAi . As a control, cells were transfected with siRNA/miRNA control followed by 4d TGFbeta treatment (mesenchymal control) or were left untreated (epithelial control). miRNA-sequencing together with mRNA-sequencing of these EMT perturbations in combination with transcription factor binding and miRNA target prediction enabled us to build an interaction map between these EMT factors.
2021-04-06 | GSE115374 | GEO
Project description:To investigate the transcriptional remodelling during EMT, we transfected normal murine mammary gland epithelial cells during a 4d TGFbeta treatment individually with siRNA against 46 transcription (co)factors or with 13 mature miRNA, all factors that blocked EMT in a phenotypic microscopy-based EMT screen upon RNAi . As a control, cells were transfected with siRNA/miRNA control followed by 4d TGFbeta treatment (mesenchymal control) or were left untreated (epithelial control). miRNA-sequencing together with mRNA-sequencing of these EMT perturbations in combination with transcription factor binding and miRNA target prediction enabled us to build an interaction map between these EMT factors.
2021-04-06 | GSE115375 | GEO
Project description:miRNA regulatory landscape of EMT [mRNA-seq]
| PRJNA474732 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2018-06-05 | GSE115376 | GEO
Project description:<p>The involvement of membrane-bound solute carriers (SLCs) in neoplastic transdifferentiation processes is poorly defined. Here, we examined changes in the SLC landscape during epithelial-mesenchymal transition (EMT) of pancreatic cancer cells. We show that two SLCs from the organic anion/cation transporter family, SLC22A10 and SLC22A15, favor EMT via interferon (IFN) α and γ signaling activation of receptor tyrosine kinase-like orphan receptor 1 (ROR1) expression. In addition, SLC22A10 and SLC22A15 allow tumor cell accumulation of glutathione to support EMT via the IFNα/γ-ROR1 axis. Moreover, a pan-SLC22A inhibitor lesinurad reduces EMT-induced metastasis and gemcitabine chemoresistance to prolong survival in mouse models of pancreatic cancer, thus identifying new vulnerabilities for human PDAC.</p>
2021-10-15 | MTBLS1925 | MetaboLights
Project description:The epithelial-mesenchymal transition (EMT) is a fundamental developmental process that is abnormally activated in cancer metastasis. Dynamic changes in alternative splicing occur during EMT. ESRP1 and hnRNPM are splicing regulators that promote an epithelial splicing program and a mesenchymal splicing program, respectively. The functional relationships between these splicing factors in the genome-scale remain elusive. Comparing alternative splicing targets of hnRNPM and ESRP1 revealed that they co-regulate a set of cassette exon events, with the majority showing discordant splicing regulation. hnRNPM discordantly regulated splicing events show a positive correlation with splicing during EMT while concordant splicing events do not, highlighting the antagonistic role of hnRNPM and ESRP1 during EMT. Motif enrichment analysis near co-regulated exons identifies guanine-uridine rich motifs downstream of hnRNPM-repressed and ESRP1-enhanced exons, supporting a model of competitive binding to these cis-elements to antagonize alternative splicing. The set of co-regulated exons are enriched in genes associated with cell-migration and cytoskeletal reorganization, which are pathways associated with EMT. Splicing levels of co-regulated exons are associated with breast cancer patient survival and correlate with gene sets involved in EMT and breast cancer subtypes. In conclusion, hnRNPM and ESRP1 co-regulate antagonistically a set of alternative splicing events that occur during EMT. This regulation is likely mediated through competition for the same intronic binding sites downstream of variable exons. hnRNPM and ESRP1 regulated splicing events are associated with breast cancer survival.
2018-08-01 | GSE112516 | GEO
Project description:Epithelial-mesenchymal transition (EMT) plays important roles in tumour progression and is orchestrated by dynamic changes in gene expression. While it is well established that post-transcriptional regulation plays a significant role in EMT, the extent of alternative polyadenylation (APA) during EMT has not yet been explored. Using 3’ end anchored RNA sequencing, we mapped the alternative polyadenylation landscape (APA) following TGF-β-mediated induction of EMT in human mammary epithelial cells and found APA generally causes 3’UTR lengthening during this cell state transition. Investigation of potential mediators of APA indicated the RNA-binding protein Quaking (QKI), a splicing factor induced during EMT, regulates a small subset of events including the length of its own transcript. Analysis of QKI CLIP-seq data identified the binding of QKI within 3’UTRs was enriched near cleavage and polyadenylation sites. Following QKI knockdown, APA of many transcripts are altered to produce predominantly shorter 3’UTRs associated with reduced gene expression. These findings reveal the changes in APA that occur during EMT and identify a potential role for QKI in this process.
2023-12-21 | GSE228929 | GEO