HaCaT cells treated with bleogen pB1 or eGF
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE202512 | GEO | 2022/09/15
REPOSITORIES: GEO
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Project description:HaCaT cells treated with bleogen pB1 or eGF
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Project description:We employed human HaCaT cells as a model system to identify cellular proteins that accompany SDS-induced toxicity based on a proteomic approach. HaCaT human keratinocyte cell line were treated with a non-cytotoxic dose of SDS (25 µg/ml, as determined by the MTT assay and microscopically examination) for 48 h. The altered abundance of proteins from HaCaT keratinocytes exposed to SDS was analyzed by LC-MS/MS approach and quantified using Progenesis LC software. The abundance of 217 proteins (which were identified by multiple peptides, ≥ 2) was altered in keratinocytes exposed to SDS; in which 131 proteins had increased abundance while 86 proteins was down regulated. The Pathview map of 131 up-regulated proteins was built and enhancement of glycolysis/gluconeogenesis was found.
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Project description:Triton X-100 has been used as a model substance to study the effects of irritants on the skin. HaCaT human keratinocyte cell line were treated with a non-cytotoxic dose of Triton X-100, as determined by the MTT assay and microscopically examination) for 48 h. The altered abundance of proteins from HaCaT keratinocytes exposed to Triton X-100 was analyzed by LC-MS/MS approach and quantified using Progenesis LC software.
2017-11-03 | PXD007776 | Pride
Project description:We performed RNA-seq on primary human keratinocytes treated with mevastatin to identify the molecular mechanisms by which statins promote wound healing. Our results identified a mevastatin gene signature that activated and modulated the EGF signaling to trigger an anti-proliferative and pro-migratory phenotype. In addition, EGFR signaling is downregulated in chronic non-healing wounds and mevastatin was able to restore EGFR signaling by downregulating caveolin proteins, a known inhibitor of EGFR signaling and wound healing. These results demonstrate that statins may have considerable therapeutic potential for patients with chronic wounds that can be rapidly translated to clinical use.
2024-06-30 | GSE137441 | GEO
Project description:We report the application of transcriptome sequencing technology in the analysis of transcriptome changes in human epidermal stem cells after EGF incubation. We found that EGF can significantly change the gene transcription of human epidermal stem cells. There are 3,759 differential genes, which are highly related to wound healing and the proliferation and differentiation of epidermal stem cells. This study provides a basis for comprehensive analysis of the effect of EGF/EGFR pathway on epidermal stem cells.
2020-08-13 | GSE156089 | GEO
Project description:Transcriptional profiling of SE-14000 stimulated wound healing associated cells (HaCat, NHDF, HMEC-1) comparing sham-treated cells. Goal was to determine the effects of SE-14000 in the human skin cells (HaCat, NHDF, HMEC-1).
2021-02-19 | GSE110830 | GEO
Project description:Constitutive activation of EGFR- and NF-kB-dependent pathways is a hallmark of cancer, yet signaling proteins that connect both oncogenic cascades are poorly characterized. Here we define KIAA1199 as a BCL-3- and p65-dependent gene in transformed keratinocytes. KIAA1199 expression is enhanced upon human papillomavirus (HPV) infection and is aberrantly expressed in clinical cases of cervical (pre)neoplastic lesions. Mechanistically, KIAA1199 binds Plexin A2 and protects from Semaphorin 3A-mediated cell death by promoting EGFR stability and signaling. Moreover, KIAA1199 is an EGFR-binding protein and KIAA1199 deficiency impairs EGF-dependent Src, MEK1 and ERK1/2 phosphorylations. Therefore, EGFR stability and signaling to downstream kinases requires KIAA1199. As such, KIAA1199 promotes EGF-mediated epithelial-mesenchymal transition (EMT). Taken together, our data define KIAA1199 as an oncogenic protein induced by HPV infection and constitutive NF-kB activity that transmits pro-survival and invasive signals through EGFR signaling. We used microarrays to detail the global programme of gene expression upon BCL-3 overexpression We used two experimental conditions, namely HaCat cells infected with a control lentivirus as well as HaCat cells infected with a BCL-3 expressing construct. Both experimental conditions were in triplicates.
2014-11-04 | E-GEOD-60551 | biostudies-arrayexpress
Project description:Human m6A-mRNA&lncRNA Epitranscriptomic Microarray of arsenite-transformed human keratinocytes (HaCaT-T cells, 1 μM arsenite exposure for 50 passages) compared to its control HaCaT cells (passed for 50 passages without arsenic exposure).
2020-11-08 | GSE161033 | GEO
Project description:Transcriptional profiling of SE-14000 stimulated wound healing associated cells (HaCat, NHDF, HMEC-1) comparing control untreated cells. Goal was to determine the effects of SE-14000 to the wound healing associated cells (HaCat, NHDF, HMEC-1).
2020-07-07 | GSE100902 | GEO
Project description:The p53 protein is encoded by TP53 gene and plays the key role in significant number of cellular processes including proliferation, apoptosis and regulation of many stress response pathways. P53 acts like a direct transcription activator of numerous genes regulating cell cycle arrest, DNA repair, growth inhibition and many others (Mollereau and Ma, 2014). The canonical biological function of p53 is maintaining genome integrity via elimination of damaged or exposed to genotoxic stress cells. Immortalized HaCaT cells are widely used for keratinocyte research, since they maintain stable keratinocyte phenotype, have nearly unlimited proliferative potential, do not require specific growth and differentiation factors (Colombo et al., 2017). Also, HaCaT cells produce typical differentiation markers such as cytokeratins K14 and K10, involucrin (Colombo et al., 2017) and respond to keratinocyte differentiation stimuli. Taking together, HaCaT cells have similar to normal human keratinocytes (NHK) properties, however, as many of spontaneously immortalized cell lines HaCaT cells bear two mutant p53 alleles - R282Q and H179Y (Lehman et al., 1993). Mutp53 in HaCaT has an increased affinity to other p53 family members (p63, p73), which significantly expands p53 properties. Moreover, mutp53 indirectly affects specific target genes via protein-protein interactions with other transcription factors (NF-Y, E2F1, NF-KB) or by tethering p63 to new promotor locations. For more detailed investigation of mutp53 impact on various processes in HaCaT cells we performed a shRNA mediated knockdown of mutp53. For generation of stable TP53 knockdown we employed plasmid vector pLKO-p53-shRNA-941 (Addgene # #25637) followed by puromycin selection of transduced cells. Here we present proteomic dataset obtained from wild type HaCaT cells and p53 knock down HaCaT keratinocytes.
2022-04-28 | PXD033538 | Pride