Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA153867 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE29724: Unsupervised hierarchical clustering of iNPCs induced by 6 or 5 TFs GSE29726: The overexpression of Pax6 affects mesenchymal to epithelial transition (MET) pathway during iPS induction in NPC. GSE29728: Overexpression of each of the 6 interfering TFs and 5 non-interfering TFs GSE29729: Selection of NPC specific Transcription factors GSE29730: Unsupervised hierarchical clustering of iHPCs induced by 9 or 10 TFs Refer to individual Series
2011-06-10 | E-GEOD-29875 | biostudies-arrayexpress
Project description:We performed a microarray analysis to compare N31EGFP and N31Pax6 transcriptional profiles 24 h after iPS induction. Among 603 genes whose levels changed greater than two-fold (295 lower, 308 higher), we noticed a 10-fold decrease in the Cdh1 signal in N31Pax6, which was confirmed by reverse transcription-mediated quantitative polymerase chain reaction (RT-QPCR). iPS induction is known to require activation of the mesenchymal to epithelial transition (MET) pathway, which involves Cdh1 upregulation. In fact, Twist1 expression, repression of which is required for MET pathway activation was higher in N31Pax6. Dox-inducible iPS-NPC, N31, was established from the primary iPSC induced from NSEB5-2C by introducing dox-inducible Oct3/4, Sox2, Klf4 and c-Myc. EGFP or Pax6 were overexpressed in N31 by transfecting CAG-EGFP-IP or CAG-Pax6-IP by Tol2 transposon. Gene expression was measured at 24 hours after exposure to doxycycline, when apparent morphological change was observed only in N31EGFP.
2011-06-07 | E-GEOD-29726 | biostudies-arrayexpress
Project description:We performed a microarray analysis to compare N31EGFP and N31Pax6 transcriptional profiles 24 h after iPS induction. Among 603 genes whose levels changed greater than two-fold (295 lower, 308 higher), we noticed a 10-fold decrease in the Cdh1 signal in N31Pax6, which was confirmed by reverse transcription-mediated quantitative polymerase chain reaction (RT-QPCR). iPS induction is known to require activation of the mesenchymal to epithelial transition (MET) pathway, which involves Cdh1 upregulation. In fact, Twist1 expression, repression of which is required for MET pathway activation was higher in N31Pax6.
2011-06-07 | GSE29726 | GEO
Project description:Background: Nephron progenitor cells (NPCs) undergo a stepwise process to generate all mature nephron structures. Mesenchymal to epithelial transition (MET) is considered a multi-step process of NPC differentiation to ensure progressive establishment of new nephrons. However, despite this important role, to date, no marker for NPCs undergoing MET in the nephron exists. Results: Here, we identify LGR6 as a NPC marker, expressed in very early cap mesenchyme, pre-tubular aggregates, renal vesicles and in segments of S-shaped bodies, following the trajectory of MET. By using a lineage tracing approach in embryonic explants in combination with confocal imaging and single-cell RNA sequencing, we provide evidence for the multiple fates of LGR6+ cells during embryonic nephrogenesis. Moreover, by using long-term in vivo lineage tracing, we show that postnatal LGR6+ cells are capable of generating the multiple lineages of the nephrons. Conclusion: Given the profound early mesenchymal expression and MET signature of LGR6+ cells, together with the lineage tracing of mesenchymal LGR6+ cells, we conclude that LGR6+ cells contribute to all nephrogenic segments by undergoing MET. LGR6+ cells can therefore be considered an early committed NPC population during embryonic and postnatal nephrogenesis with potential regenerative capability.
2021-05-25 | GSE164795 | GEO
Project description:This paper shows, for the first time, a novel function of the OVO-like proteins (OVOL1and OVOL2) as critical inducers of mesenchymal to epithelial transition (MET) in human cancer. Examination of the effects of OVOL1 and OVOL2 overexpression in a prostate cancer model.
2013-08-01 | E-GEOD-48230 | biostudies-arrayexpress
Project description:The metastasis of nasopharyngeal carcinoma (NPC) is a complex process associated with oncogenic dysfunction, the deciphering of which remains a challenge and requires more in-depth studies. Y-box protein 3 (YBX3) is a DNA/RNA binding protein associated with gene transcription, DNA repair and the progression of various diseases. However, whether and how YBX3 affects the metastasis of NPC remains unknown. Thus, in this study, we aimed to investigate the role of YBX3 in the metastasis of NPC and determine its underlying mechanism. Interestingly, it was found that the expression of YBX3, which was associated with NPC metastasis, was upregulated in the clinical NPC tissues and cell lines using solid experimental evidences. Moreover, we found that knockdown of YBX3 expression by lentivirus shRNA significantly suppressed NPC cells migration in vitro and metastasis in vivo. Mechanistically, RNA sequencing results suggested that the genes regulated by YBX3 were significantly enriched in cell adhesion molecules, cAMP signaling pathway, calcium signaling pathway, focal adhesion, PI3K-Akt signaling pathway, Ras signaling pathway, Rap1 signaling pathway, NF-κB signaling pathway, and Chemokine signaling pathway. Of these, PI3K-Akt signaling pathway contained the most genes. Accordingly, YBX3 knockdown decreased the activation of PI3K/AKT signaling, thereby inhibit epithelial-to-mesenchymal transition and MMP1. These results have demonstrated that YBX3 are involved in the metastasis of NPC through regulating PI3K/AKT signaling pathway, and serve as a potential therapeutic target for patients with NPC.
2021-04-07 | GSE160245 | GEO
Project description:<p>Nasopharyngeal carcinoma (NPC) is an aggressive head and neck cancer characterized by Epstein-Barr virus (EBV) infection and dense lymphocyte infiltration. The scarcity of NPC genomic data hinders the understanding of NPC biology, disease progression, and rational therapy design. Here, we performed whole-exome sequencing (WES) on 111 micro-dissected EBV-positive NPCs, with 15 cases subjected to further whole-genome sequencing (WGS), to determine its mutational landscape. We identified enrichment for genomic aberrations of multiple negative regulators of the NF-kB pathway in a total of 41% of cases including CYLD, TRAF3, NFKBIA and NLRC5. Functional analysis confirmed novel inactivating CYLD mutations as drivers for NPC cell growth. The EBV oncoprotein latent member protein 1 (LMP1) functions to constitutively activate NF-kB signaling, and we observed mutual exclusivity among somatic NF-kB pathway aberrations and LMP1-overexpression, suggesting that NF-kB activation is selected for by both somatic and viral events during NPC pathogenesis.</p>
| phs001244 | dbGaP
Project description:How disseminated tumor cells (DTCs) engage specific stromal components in distant organs for survival and outgrowth is a critical but poorly understood step of the metastatic cascade. Previous studies have demonstrated the importance of the epithelial-mesenchymal transition (EMT) in promoting the cancer stem cell properties needed for metastasis initiation, while the reverse process of mesenchymal-epithelial transition (MET) is required for metastatic outgrowth. Here we report that this paradoxical requirement for simultaneous induction of both MET and cancer stem cell traits in DTCs is provided by bone vascular niche E-selectin. Using cell surface alkoxyamine-biotinylation and label-free LC-MS/MS, Glg1 was identified as a top candidate Fut3/Fut6-dependent E-selectin ligand. We functionally validated their involvement in the formation of bone metastasis. These findings provide unique insights into the functional role of E-selectin as a component of the vascular niche criticalfor metastatic colonization in bone.
2019-11-13 | PXD012942 | Pride
Project description:Epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) facilitate breast cancer (BC) metastasis, however stable molecular changes that result as a consequence of these processes remain poorly defined. Therefore, we sought to identify molecular markers that could distinguish tumor cells that had completed the EMT:MET cycle in the hopes of identifying and targeting unique aspects of metastatic tumor outgrowth.Therefore, normal murine mammary gland (NMumG) cells transformed by overexpression of EGFR (NME) cells were cultured in the presence of TGF-beta1 (5 ng/ml) for 4 weeks, at which point TGF-beta1 supplementation was discontinued and the cells were allowed to recover for an additional 4 weeks (Post-TGF-Rec). Total RNA was prepared from unstimulated cells (Pre-TGF) of similar passage and compared by microarray analysis. The two groups were analyzed in triplicate, three Pre-TGF samples and three Post-TGF-Rec samples.
2014-01-30 | E-GEOD-54491 | biostudies-arrayexpress
Project description:The aggregation of nephron progenitor cells (NPC) is required to form the nephron precursor renal vesicle (RV) as they undergo the mesenchymal-to-epithelial transition (MET). Canonical Wnt signaling regulates the MET of NPCs via the effector molecule β-catenin. β-catenin acts as a transcriptional co-activator during the differentiation of NPCs, however, if it has any role as an adhesion regulating molecule via the cadherin-catenin complex is currently unknown. Using in vitro NPC culture system with gene editing and modulated Wnt signaling input, we investigated the morphological transition of NPCs and its underlying mechanism modeling the initial step of the MET in vivo. Increasing Wnt signaling input with the small molecule agonist CHIR resulted in the aggregation of NPCs similar to the generation of the nephron anlagen. By removing β- and α-catenin from the NPCs, NPCs are sorted out from these aggregates, demonstrating the key role of the cadherin-catenin complex in the aggregation. β-catenin was essential for the induction, however, the removal of α-catenin did not affect the transcriptional profile of NPCs. Removal of extracellular Ca2+ resulted in the transient loss of cell-cell contacts suggesting the role of cadherins in the aggregation process. The analysis of in vitro bulk RNA-seq cadherin expression profile matched the in vivo cadherin expression profile determined by single-cell RNA-seq. The combined removal of pre-existing and inducible cadherins phenocopied the results of β- and α-catenin KO experiments highlighting the crucial role of the cadherin-catenin complex by multiple lines of evidence. Notably, the induction of NPCs is independent of their aggregation. The in vitro modeling of nephron development provides a mechanistic understanding how cell adhesion is regulated via the cadherin-catenin complex during nephrogenesis.
2024-07-29 | GSE232606 | GEO