Similar Datasets
Project description:HEK siRNA vs. HEK control<br>HeLA siRNA vs. HeLa control
2010-02-25 | E-MEXP-2591 | biostudies-arrayexpress
Project description:The study aimed to interrogate whether the 1,4-naphtoquinone derivative lawsone activates the aryl hydrocarbon receptor (AhR) downstream transcriptional program in keratinocytes and is capable of modulating skin homeostasis. The study has been performed on human primary epidermal keratinocytes (HEKs), which represent the first line of defense against exogenous molecules. HEK cells were treated with the vehicle control DMSO (control), stimulated with lawsone or with the TLR2 ligand Pam2CSK4. Transcriptional profiles of HEK cells were studied to investigate the regulation of AhR -related genes, Nrf2-related genes and epidermal differentiation and keratin genes. We demonstrated that lawsone was sensed by keratinocytes and activated AhR. In particular, lawsone efficiently activated the transcriptional program of AhR and promoted keratinocyte differentiation.
2019-08-06 | GSE99901 | GEO
Project description:In order to understand the transcriptional effects of CD44s expression in a cell line that does not express CD44 in its native form we transfected CD44s into HEK cells and measured the transcriptional chances compared to native HEK cells
2014-12-05 | GSE63862 | GEO
Project description:HEK 293 cells were infected with Adenovirus expressing cDNA of PTTG gene. A control cells infected with Adenovirus without PTTG gene cDNA were used.
2009-12-31 | E-MEXP-2449 | biostudies-arrayexpress
Project description:Long non-coding RNAs (lncRNAs) have gained widespread attention as a potential new layer of regulation in biological processes during development and disease. The lncRNA ELDR (EGFR long non‐coding downstream RNA) was recently shown to be highly expressed in oral cancers as compared to adjacent non-tumor tissue, and we previously reported that ELDR may be an oncogene as inhibition of ELDR reduces tumor growth in oral cancer models. Furthermore, overexpression of ELDR induces proliferation and colony formation in normal oral keratinocytes (NOKs). In this study, we examined in further detail how ELDR drives the neoplastic transformation of normal keratinocytes. We performed RNA-seq analysis on NOKs stably expressing ELDR (NOK-ELDR), which revealed that ELDR enhances the expression of cell cycle-related genes. Increased expression of Aurora kinase A (AURKA) and its downstream gene targets Polo-Like Kinase 1 (PLK1), Cell Division Cycle 25C (CDC25C), Cyclin-Dependent Kinase 1 (CDK1), and Cyclin B1 (CCNB1) are significantly increased in NOK-ELDR cells, suggesting induction of G2/M progression. We further identified CCCTC-Binding Factor (CTCF) as a binding partner of ELDR in NOK-ELDR cells. We showed that ELDR stabilizes CTCF and increases its expression. Finally, we demonstrate the ELDR-CTCF axis upregulates transcription factor Forkhead Box M1 (FOXM1), which induces AURKA expression and downstream G2/M transition. These findings provide mechanistic insights into the role of the lncRNA ELDR as a potential driver of oral cancer during neoplastic transformation of normal keratinocytes.
2022-05-11 | GSE198818 | GEO
Project description:A cell supsension containing an equal mix of HEK and 3T3 cells was used in the Fluidigm C1
2015-06-24 | GSE70151 | GEO
Project description:The oral cavity is the persistent reservoir for EBV with lifelong infection of resident epithelial and B cells. Infection of these cell types results in distinct EBV gene expression patterns that are regulated by epigenetic modifications involving DNA methylation and chromatin structure. Such regulation of EBV gene expression relies on viral manipulation of the host epigenetic machinery that may inadvertently result in long-lasting, oncogenic host epigenetic reprogramming. To test this hypothesis in the context of EBV infection of epithelial cells, we established a transient infection model to identify the epigenetic consequences after EBV infection of immortalized normal oral keratinocytes and subsequent viral loss. With mounting evidence that EBV can induce epigenetic alterations, we developed a transient infection model where a clonal derivative (designated cl1) from a human telomerase immortalized normal oral keratinocyte (NOK) cell line was infected with a recombinant Akata EBV carrying neomycin resistance and GfP cassette in place of the BXLF1 open reading frame. Infected cells were passaged ten times, and then selection pressure was removed for an additional ten passages to allow for viral loss. Three transiently-infected EBV-negative clones were identified by single cell cloning (designated cl1, cl3, cl4). Uninfected parental clone and cells transfected with PTRUF5 plasmid were passaged alongside the transiently-infected clones. The transcription profiles were analyzed using Affymetrix microarray U133Plus2.0 arrays in duplicate. NOK cells were single cell cloned (designated as cl1) and EBV infected by co-culture with a recombinant Akata EBV strain carrying neomcycin resistance and GFP expression cassette in place of EBV BXLF1. Cells were selected with 350 ug/ml G418. As a selection control, cells were transfected a plasmid carrying a neomycin resistance cassette. Cells were passaged 10 times with G418, followed by removal of selection pressure. After an additional 10 passages, cells were single cell cloned and the presence of EBV was determined by various methods. Three clones were identified as being EBV negative and said to be transiently infected. Uninfected parental and vector transfected cells were passaged in the same manner and also single cell cloned.
2014-08-01 | E-GEOD-58914 | biostudies-arrayexpress
Project description:In order to understand the transcriptional effects of CD44s expression in a cell line that does not express CD44 in its native form we transfected CD44s into HEK cells and measured the transcriptional chances compared to native HEK cells Three biological replicates from each condition (native HEK cells and CD44s transfected cells) were measured using Affymetrix arrays
2014-12-05 | E-GEOD-63862 | biostudies-arrayexpress
Project description: Not available
| S-EPMC5376294 | biostudies-literature