GRHL3 activates FSCN1 to relax cell adhesions between migrating keratinocytes in the wound front
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE172161 | GEO | 2021/10/13
REPOSITORIES: GEO
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Project description:GRHL3 activates FSCN1 to relax cell adhesions between migrating keratinocytes in the wound front
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Project description:The migrating keratinocyte wound front is required for skin wound closure. Despite significant advances in wound healing research, we do not fully understand the molecular mechanisms that orchestrate collective keratinocyte migration. Here, we show that, in the wound front, the epidermal transcription factor Grainyhead like-3 (GRHL3) mediates decreased expression of the adherens junction protein E-cadherin; this results in relaxed adhesions between suprabasal keratinocytes, thus promoting collective cell migration and wound closure. Wound fronts from mice lacking GRHL3 in epithelial cells (Grhl3-cKO) have lower expression of Fascin-1 (FSCN1), a known negative regulator of E-cadherin. Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq) on wounded keratinocytes shows decreased wound-induced chromatin accessibility near the Fscn1 gene in Grhl3-cKO mice, a region enriched for GRHL3 motifs. These data reveal a wound-induced GRHL3/FSCN1/E-cadherin pathway that regulates keratinocyte-keratinocyte adhesion during wound-front migration; this pathway is activated in acute human wounds and is altered in diabetic wounds in mice, suggesting translational relevance.
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Project description:To investigate the RNA binding property of FSCN1 in ESCC, RNA immunoprecipitation (RIP) was performed using an FSCN1 monoclonal antibody in ECA-109 cell lysate
2022-03-05 | GSE197621 | GEO
Project description:Fascin actin-bundling protein 1 (FSCN1) is an evolutionarily conserved actin-bundling protein that plays a critical role in cell migration, motility, adhesion and cellular interactions. Although multiple clinical studies have implicated the expression of FSCN1 in laryngeal squamous cell carcinoma (LSCC) progression, the precise mechanism of FSCN1 in the process has not been clearly elucidated. To define FSCN1 function, we characterized FSCN1-interacting proteins in LSCC cells by immunoprecipitation followed by LC-MS/MS. After data filtering, 119 proteins with expression in both the Hep-2 and TU-177 cell samples were identified as FSCN1-interacting partners. With in-depth bioinformatics analysis, we linked FSCN1 to critical cellular processes including cell adhesion, glycolysis/gluconeogenesis, regulation of protein ubiquitination, ribosomal RNA processing and small molecule metabolism. We discuss the interactions between FSCN1 and some of the newly validated partners. The identification of these potential partners of FSCN1 expands our knowledge of the FSCN1 interactome and provides a valuable resource for understanding the functions of this protein in LSCC progression.
2019-09-09 | PXD013072 | Pride
Project description:The actin-bundling protein fascin (FSCN1) is overexpressed in aggressive adrenocortical carcinoma (ACC) and represents a reliable prognostic indicator. We investigated the effects of FSCN1 inactivation by CRISPR/Cas9 in ACC H295R cells on global gene expression profiles in those cells. We performed gene expression profiling analysis using data obtained from RNA-seq of 2 different H295R control clones and 2 different FSCN1 KO clones (2 biological replicates for each clone).
2022-10-25 | GSE216008 | GEO
Project description:To explore the downstream molecules of FSCN1, shRNA targeting FSCN1 was designed and transfected into the ESCC cell line, ECA-109. Whole-genome expression profiling was performed to screen for related molecules. To investigate the RNA binding property of FSCN1 in ESCC, RNA immunoprecipitation (RIP) was performed using an FSCN1 monoclonal antibody in ECA-109 cell lysate, and the associated RNA was analyzed by RNA-seq.
2022-03-05 | GSE197624 | GEO
Project description:FSCN1 has been reported to be dysregulated in cervical cancers. However, the genome-wide regulated targets of FSCN1 is still unclear in cervical cancers. Here, the gene expression profile of HeLa cells transfected with FSCN1 shRNA (shFSCN1) were compared with cells transfected with empty vector (shCtrl). The results showed that shFSCN1 extensively affects the transcriptional level of 5, 043 genes in HeLa cells. There were more up-regulated genes (3, 870) than down-regulated ones (1, 173) after FSCN1 was knocked down in HeLa cells. GO analysis showed that the up-regulated genes were associated with transcription regulation and DNA binding. The down-regulated genes were enriched in some cancer associated pathway including angiogenesis and cell adhesion. In particular, FSCN1 positilvely regulated ANGPTL4 in HeLa cells. Compared to normal tissue, both FSCN1 and ANGPTL4 showed a higher expression in cervical tumor tissue. Moreover, ANGPTL4 was also positilvely correlated with expression of FSCN1 in cervical tumor tissue of TCGA. In conclusion, our study provide important cues for further study on the regulatory mechanism of FSCN1 in cervical cancer.
2022-01-20 | GSE149450 | GEO
Project description:The antagonistic actions of Polycomb and Trithorax are responsible for proper cell fate determination in mammalian tissues. In the epidermis, a self-renewing epithelium, previous work has shown that release from Polycomb repression only partially explains differentiation gene activation. We now show that Trithorax is also a key regulator of epidermal differentiation, not only through activation of genes repressed by Polycomb in progenitor cells, but also through activation of genes independent of regulation by Polycomb. The differentiation associated transcription factor GRHL3/GET1 recruits the ubiquitously expressed Trithorax complex to a subset of differentiation genes. Examination of WDR5 and GRHL3 binding in human differentited primary keratinocytes (NHEK). High calcium medium was added to NHEK cells at 50% confluency to induce differentiation. Cells were collected for ChIP 24 hours after addition of high calcium medium. ChIP with Wdr5 and Grhl3 antibodies, and an input control were sequenced.
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Project description:Grainyhead-like transcription factor 3 (GRHL3) is known to affect cancer development depending on subtypes in various entities. Here, we analyzed the subtype-specific role of GRHL3 in bladder carcinogenesis comparing common urothelial carcinoma (UC) with squamous bladder cancers (sq-BLCA). We examined GRHL3 mRNA and protein expression in cohorts of patient samples, its prognostic role as well as its functional impact on tumorigeneses in different molecular and histopathological subtypes of bladder cancer. We showed for GRHL3 a reverse expression in squamous and urothelial bladder cancer subtypes. Stably GRHL3 overexpressing EJ28 and SCaBER in vitro models revealed a tumor suppressive function in squamous and a oncogenic role in the urothelial cancer cells affecting cell migratory and invasive capacities. Transcriptomic profiling demonstrated highly subtype specific GRHL3 regulated expression networks coined by enrichment of genes involved in integrin mediated pathways. In SCaBER loss of RhoA GTPase activity was demonstrated associated with co-regulation of EIF4E3, a potential tumor suppressor gene. Thus, our data provide for the first time a detailed insight into the role of the transcription factor GRHL3 in different histopathological subtypes of bladder cancer.
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