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E-MEXP-1389

ABSTRACT: Transcription profiling by array of human HL60 cells treated with eicosapantaenoic acid (EPA) to investigate the effect on the signalling pathways involved in growth arrest/apoptosis

PROVIDER: E-MEXP-1389 | ExpressionAtlas | 2025-01-22

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-MEXP-1389-analysis-methods.tsv	Tabular
	E-MEXP-1389-atlasExperimentSummary.Rdata	Rdata
	E-MEXP-1389-configuration.xml	Xml
	E-MEXP-1389-percentile-ranks.tsv	Tabular
	E-MEXP-1389.condensed-sdrf.tsv	Tabular

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Transcription profiling by array of human HL60 cells treated with eicosapantaenoic acid (EPA) to investigate the effect on the signalling pathways involved in growth arrest/apoptosis

Project description:We investigated the effect of EPA on the signalling pathways involved in growth arrest/apoptosis in HL60 cells. EPA inhibited cell proliferation in HL60 cells in a dose dependent manner. Gene expression profiling of HL60 cells treated with EPA was performed by Affymetrix GeneChip. System and key markers of relevant pathways were verified at protein level by western blotting.

2008-11-11 | E-MEXP-1389 | biostudies-arrayexpress

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Genome-wide analysis of fatty acid synthase (FASN) gene silenced retinoblastoma cancer cells (WERI RB1) using cDNA microarray analysis

Project description:Fatty acid synthase is a major enzyme involved in de novo lipogenesis and associated with tumor invasion and poor prognosis. The effect of fatty acid synthase knockdown in retinoblastoma cancer cells (WERI RB1) using siRNA mediated gene silencing were accessed for global gene deregulations. The analysis resulted in RB cancer cell death through deregulations of various cell signalling, metabolic, immunity, angiogenesis, apoptosis and cell cycle pathway related genes. Further validations were done using qRT-PCR and western analysis. Our results provide evidence that blockade in lipid metabolism inturn lead to RB cancer cell death through impaired cell signalling pathway.

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Expression data for triple-negative breast cancer (TNBC) cells following chemotherapy

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Gene expression data from differentiated 3T3-L1 preadipocytes treated with Palmitic Acid, Stearic Acid, Palmitoleic Acid, or Oleic Acid

Project description:Saturated fatty acids (SFA) are widely thought to induce inflammation in adipose tissue (AT), while monounsaturated fatty acids (MUFA) are purported to have the opposite effect; however, it is unclear if individual SFA and MUFA behave similarly. Our goal was to examine adipocyte transcriptional networks regulated by individual SFA (palmitic acid, PA; stearic acid, SA) and MUFA (palmitoleic acid, PMA; oleic acid, OA). Global gene expression was examined in differentiated preadipocytes treated with either 250 μM PA, SA, PMA, or OA for 48 hrs. Individual fatty acid treatments had significant effects on adipocyte gene expression. Functional analyses revealed that PA induced the TLR signalling pathway, while PMA had the opposite effect. SA and OA had similar effects, with increases in key metabolic pathways including mTOR and PPAR signalling, and a reduction in TLR signalling. Ccl5 was validated as a candidate gene that may mediate the differential inflammatory effects of SFA and MUFA in AT. Individual SFA and MUFA trigger distinct transcriptional responses in differentiated preadipocytes, with inflammatory and metabolic pathways particularly sensitive to these fatty acids.

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Host-defence peptides caerin 1.1 and 1.9 stimulate TNF-alpha-dependent apoptosis in human cervical cancer HeLa cells

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Project description:Retinoic acid (RA) signalling is an important regulator of lung development and repair. To investigate the molecular mechanisms underlying RA-mediated responses in lung endothelial cells, we profiled the gene expression of human pulmonary microvascular endothelial cells (HPMECs) treated with RA or ethanol (EtOH) vehicle control. Whole-genome expression analysis using Affymetrix Human U133 Plus 2.0 GeneChips identified transcriptional changes associated with angiogenesis, wound healing, and signalling pathways relevant to alveolar repair.

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Gene expression data from differentiated 3T3-L1 preadipocytes treated with Palmitic Acid, Stearic Acid, Palmitoleic Acid, or Oleic Acid

Project description:Saturated fatty acids (SFA) are widely thought to induce inflammation in adipose tissue (AT), while monounsaturated fatty acids (MUFA) are purported to have the opposite effect; however, it is unclear if individual SFA and MUFA behave similarly. Our goal was to examine adipocyte transcriptional networks regulated by individual SFA (palmitic acid, PA; stearic acid, SA) and MUFA (palmitoleic acid, PMA; oleic acid, OA). Global gene expression was examined in differentiated preadipocytes treated with either 250 M-NM-<M PA, SA, PMA, or OA for 48 hrs. Individual fatty acid treatments had significant effects on adipocyte gene expression. Functional analyses revealed that PA induced the TLR signalling pathway, while PMA had the opposite effect. SA and OA had similar effects, with increases in key metabolic pathways including mTOR and PPAR signalling, and a reduction in TLR signalling. Ccl5 was validated as a candidate gene that may mediate the differential inflammatory effects of SFA and MUFA in AT. Individual SFA and MUFA trigger distinct transcriptional responses in differentiated preadipocytes, with inflammatory and metabolic pathways particularly sensitive to these fatty acids. A total of 4 microarrays were run for each FA treatment. We experienced difficulties with the cRNA amplification for one replicate from the OA treated cells; therefore this treatment group only had an n=3. For each sample, 100 ng of total RNA was prepared for hybridization to Affymetrix Mouse Gene 1.1 ST array strips, according to the manufacturerM-bM-^@M-^Ys instructions (Affymetrix Inc., Fremont, CA, USA).

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Simvastatin modulates osteogenic differentiation in stem cells isolated from apical papilla

Project description:Background Simvastatin modulates numerous stem cell functions, including stemness maintenance and differentiation. The present study aimed to explore the effect of simvastatin on the osteogenic differentiation of SCAPs in vitro. Methods Cells were isolated from apical papilla, and mesenchymal stem cell features were characterised. Cells were treated with various concentrations of simvastatin (100-1,000 nM). The mRNA expression profile of simvastatin-treated SCAPs was examined using RNA sequencing technique. The osteogenic differentiation abilities were assessed. Alkaline phosphatase activity was determined. The mineralisation was visualised using Alizarin Red S and Von Kossa staining. The osteogenic marker gene expression was determined using a quantitative polymerase chain reaction. Results RNA sequencing data demonstrated that simvastatin upregulated genes enriched in those pathways involving osteogenic differentiation, including the TGF-beta signalling pathway, FoxO signalling pathway, and MAPK signalling pathway, while the downregulated genes were involved in pathways related to cell proliferation and apoptosis, for example, DNA replication, cell cycle, and p53 signalling pathway. Simvastatin promoted mineral deposition in a dose-dependent manner, corresponding with the upregulation of osteogenic marker genes namely OSX, DMP1, DSPP, and OCN. Pretreatment with TGF-beta receptor inhibitor, SB431542, resulted in a moderately attenuated effect on simvastatin-induced mineralisation and osteogenic marker gene expression. Conclusions Simvastatin enhances osteogenic differentiation in SCAPs, potentially via TGF-beta signalling, implicating its potential role as an adjunctive molecule in dental pulp healing and regeneration in vital pulp treatment approaches.

2025-01-22 | GSE286540 | GEO

Expression data for triple-negative breast cancer (TNBC) cells following chemotherapy

2015-07-10 | GSE70690 | GEO