Transcriptome analysis of methylparaben treated H1299 lung carcinoma cells
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ABSTRACT:
PROVIDER: PRJNA560363 | ENA |
REPOSITORIES: ENA
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Project description:Purpose: finding differential transcripts usage in environmentally harzardous chemical, methylparaben Methods: transcriptome analysis by the RNA-seq via mRNA pull-down Results: We found that methylparaben increases cellular toxicity in H1299 cells. Also, over thousands of retained intron events were detected from the RNA-seq analysis. Conclusions: Methylparaben increases cytotoxic effects in H1299 cells through the caspase-3 pathway and changes the context of trascript through the splicing regulation mechanisms.
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Project description:Purpose: finding differential transcripts usage in environmentally harzardous chemical, mercury chloride (HgCl2) in human non-small cell lung carcinoma cells Methods: transcriptome analysis by the RNA-seq via mRNA pull-down Results: We found that HgCl2 increases cellular toxicity by the increasing of apoptosis via caspase-3 independent pathway in H12999 cells. Also, over thounds of altered gene expression pattern were detected from the RNA-seq analysis. Conclusions: mercury chloride (HgCl2) increases cytotoxic effects and apoptosis in H1299 cells through the caspase-3 independent pathway and changes the context of trascript
2021-03-10 | GSE163937 | GEO
Project description:Transcriptome analysis of mercury chloride (HgCl2) treated H1299 human non-small cell lung carcinoma cells
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Project description:Transcriptional profiling of H1299 non-small cell lung carcinoma cells transfected with either wt p53 or mut(175) p53 driven by the 5xHRE promoter (5 repeats of hypoxia-inducible factor response elements) and treated for 16 h with normoxia (21% O2) or hypoxia(<0.1% O2). 5xHRE promoter ensures that p53 expression is induced in hypoxic conditions only. Goal was to determine the transcriptional response of p53 in hypoxia and the 175 p53 mutant was used as a control as it is DNA-binding defective and transcription-incompetent mutant. Four-condition experiment: wt p53-transfected H1299 cells treated with normoxia, mut p53-transfected H1299 cells treated with normoxia, wt p53-transfected H1299 cells treated with hypoxia, mut p53-transfected H1299 cells treated with hypoxia. Biological replicates: 1 normoxic sample with wt p53, 1 normoxic sample with mut p53, 3 hypoxic samples with wt p53, 3 hypoxic samples with mut p53.
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Project description:To investigate the molecular pathway signature responsive to pharmacological inhibition of USP7, we analyzed transcriptome in P22077 (a USP7 selective inhibitor)-treated H1299 and HeLa cells.
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Project description:The integral role of p53 in tumor suppression has promted many laboratories to perform extensive analyses of signaling pathways downstream of the p53 family of sequence-specific DNA binding transcription factors (p53 and its homologs p63 and p73). Despite the ability of p73 to regulate many p53 family target genes, little is known about the specific pathways that modulate p73 during development, tumorigenesis and tumor therapy. In this study we present a gene signature-based approach for connecting signaling pathways to transcription factors, as exemplified by p73. We generated a p73 gene signature by integrating whole-genome chromatin immunoprecipitation and expression profiling. Experiment Overall Design: H1299 lung carcinoma cells were transduced with TAp73beta or GFP expressing adenoviruses. Microarray analysis (on the GFP and TAp73beta samples) and ChIPSeq analysis (on the TAp73beta sample) were performed to identify candidate p73 target genes.
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Project description:Transcriptional profiling of H1299 non-small cell lung carcinoma cells transfected with either wt p53 or mut(175) p53 driven by the 5xHRE promoter (5 repeats of hypoxia-inducible factor response elements) and treated for 16 h with normoxia (21% O2) or hypoxia(<0.1% O2). 5xHRE promoter ensures that p53 expression is induced in hypoxic conditions only. Goal was to determine the transcriptional response of p53 in hypoxia and the 175 p53 mutant was used as a control as it is DNA-binding defective and transcription-incompetent mutant.
2014-01-08 | GSE53893 | GEO
Project description:To identify a set of genes related to radioresistance, we analyzed the time-series gene expression profiles of radioresistant H1299 and radiosensitive H460 lung cancer cells in response to 2 Gy of ionizing radiation (IR) by performing quadratic regression (QR) analysis. Out of the 21,331 genes, we selected 6,538 genes by QR analysis from the gene expression profile of H460 cells and 6,086 genes from that of H1299 cells. Most of the genes identified in the H460 cells were classified into continuously up- or down-regulated groups, while the major QR groups were transiently changed groups in the H1299 cell line. From gene ontology analysis of the major QR groups, the DNA damage response was commonly enriched in both cell lines. DNA repair-related genes such as ATM, ATR, TP53BP1, BRCA1, MRE11, NBN and RAD50 were particularly up-regulated in H1299 cells. Suppression of these DNA repair-related genes using siRNA made H1299 cells radiosensitive to ionizing radiation. The data suggest that differential responses to DNA damage confer radioresistance to cancer cells, and provide potential novel targets for sensitizing radiotherapy.
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