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Differential miRNA and mRNA Expression in Immortalized Human Keratinocytes (HaCaT) after Low Arsenic Exposure [mRNA]

ABSTRACT: Determining the miRNA and mRNA expression profiles in HaCaT cells at early and late stages of arsenite exposure to reveal early and late changes in the HaCaT cells transformation process.

ORGANISM(S): Homo sapiens

PROVIDER: GSE97303 | GEO | 2018/01/23

REPOSITORIES: GEO

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Differential miRNA and mRNA Expression in Immortalized Human Keratinocytes (HaCaT) after Low Arsenic Exposure [miRNA]

Project description:Determining the miRNA and mRNA expression profiles in HaCaT cells at early and late stages of arsenite exposure to reveal early and late changes in the HaCaT cells transformation process.

2018-01-23 | GSE97305 | GEO

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Protein dataset of immortalized HaCaT cells p53 knock down HaCaT keratinocytes

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

The N6-methyadenosine (m6A) levels in HaCaT-T cells and control HaCaT cells

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).

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Aberrantly expressed genes in HaCaT keratinocytes chronically exposed to arsenic trioxide

Project description:The purpose of this study is to search for aberrant genes in HaCaT keratinocytes after chronic exposure to arsenic trioxide. The objective of the investigation was to discover the mechanism of arsenic carcinogenicity in human epidermal keratinocytes. We hypothesize that a combined strategy of DNA microarray, qRT-PCR and gene function annotation will identify aberrantly expressed genes in HaCaT keratinocyte cell line after chronic treatment with arsenic trioxide. HaCaT cells were chronically exposed to 0.5M-BM-5g/mL arsenic trioxide (As2O3) up to 22 passages and RNA was extracted. Microarray data analysis identified 14 up-regulated genes and 21 down-regulated genes in response to arsenic trioxide Two experimental groups: 1. The treatment group was sub-cultured up to passage 22 to establish a chronic exposure state. 2. The passage control group was also sub-cultured up to 22 passages but with no exposure to arsenic trioxide. 4 technical replicates with 3 replicates making a total of 8X3 =24 samples HaCat Cell untreated (passage control): 1. H1_H001, H1_H002, H1_H003 2. H2_ H004, H2_H005, H2_H006 3. H3_ H007, H3_H008, H3_H009 4. H4_ H010, H4_H011, H4_H012 HaCat Cell treated with 0.5M-BM-5g/ml of arsenic trioxide: 5. A1_H013, A1_H014, A1_H015 6. A2_H016, A2_H017, A2_H018 7. A3_H019, A3_H020, A3_H021 8. A4_H022, A4_H023, A4_H024 Cell Type: Human Skin Keratinocyte: 1.5 M-CM-^W105 HaCaT cells were cultured in 7.5 ml of complete DMEM containing 10% Fetal Bovine Serum (FBS) and 1% penicillin, streptomycin in T-25 culture plate. Cells were incubated in a humidified atmosphere with 5% CO2 at 37 M-BM-:C. The treatment groups were exposed to 0.5M-BM-5g/mL As2O3 (equivalent to LC 0.5), and passaged at 90% confluent. Total RNA was extracted from 4 technical replicates of unexposed HaCaT cells and HaCaT cells chronically exposed to arsenic trioxide up to passage 22 using RNA STAT-60 (TEL-TEST, INC, Friendswood, TX, USA).

2012-04-11 | E-GEOD-37192 | biostudies-arrayexpress

Aberrantly expressed genes in HaCaT keratinocytes chronically exposed to arsenic trioxide

2012-04-12 | GSE37192 | GEO

Differential miRNA and mRNA Expression in Immortalized Human Keratinocytes (HaCaT) after Low Arsenic Exposure

Project description:Differential miRNA and mRNA Expression in Immortalized Human Keratinocytes (HaCaT) after Low Arsenic Exposure

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Influence of alkyl-phospholipids on the gene expression profile of immortalized keratinocytes HaCaT

Project description:New alkyl-phospholipids (APLs) that are structurally derived from the platelet-activating factor are promising candidates for anticancer treatment. After the incorporation into cell membranes, APLs are able to interfere with a wide variety of key enzymes implicated in cell growth, motility, invasion and apoptosis. Besides the prototype edelfosine, we presented a novel group of APLs, glycosidated phospholipids that efficiently inhibit cell proliferation. Two members of this group, Ino-C2-PAF and Glc-PAF, display high efficacy and low cytotoxicity in immortalized non-tumorigenic skin keratinocyte cell line HaCaT. However, the influence of APLs on the transcription of the whole genome is still unknown. Here, using Agilent cDNA microarray technology, we compared global gene expression profiles of HaCaT cells treated with edelfosine, Ino-C2-PAF or Glc-PAF with the profile of control cells. The influence of APLs on the transcriptional profile of immortalized keratinocytes (HaCaT) was analyzed treating HaCaT cells with respectively 5 M-BM-5M Ino-C2-PAF, Glc-PAF and edelfosine for 24 h. Control cells were left untreated. Three independent experiments were performed for each condition.

2011-03-01 | E-GEOD-20722 | biostudies-arrayexpress

Differential miRNA and mRNA Expression in Immortalized Human Keratinocytes (HaCaT) after Low Arsenic Exposure

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-01-23 | GSE97306 | GEO