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Detecting the whole genomic binding of PARP1 in H1975 cells with CUT&Tag assay.

ABSTRACT: To elucidate the mechanism of EGFR-AS1 on PARP1-DNA binding at genome level, we examined PARP1 binding in response to etoposide stimulation through CUT&Tag technique in H1975 cells which overexpressing EGFR-AS1.

ORGANISM(S): Homo sapiens

PROVIDER: GSE285816 | GEO | 2025/11/17

REPOSITORIES: GEO

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Detecting the whole genomic binding of PARP1 in H1975 cells with CUT&Tag assay.

Project description:Detecting the whole genomic binding of PARP1 in H1975 cells with CUT&Tag assay.

| PRJNA1206139 | ENA

Human lung adenocarcinoma NCI-H1975 cells: parental vs cell lines resistant to the EGFR-TK inhibitor CNX-2006

Project description:Genome variation profiling of lung adenocarcinoma cells comparing untreated NCI-H1975 cells with CNX-2006-resistant untreated cells. Goal was to determine the potential mechanism of resistance to mutant EGFR-TKIs and rationally design novel strategies for the treatment of EGFR-mutant lung cancer patients. Two-condition experiment: NCI-H1975 parental cells vs CNX-2006-resistant cells. Pooled DNA from healthy volunteers was used as reference.

2015-07-01 | E-GEOD-53234 | biostudies-arrayexpress

Characterization of parental and erlotinib-resistant derived H1975 cell lines

Project description:Through development of an in vivo orthotopic lung cancer model, we reveal an unanticipated pathway driving spontaneous metastasis that is orchestrated by the developmentally-regulated transcriptional repressor, Capicua (CIC). RNAseq and DNA copy number analysis of H1975 (EGFR-mutant lung adenocarcinoma) cells in the context of drug resistance to erlotinib

2015-11-19 | E-GEOD-74866 | biostudies-arrayexpress

Transcriptome profiling of Anlotinib-resistant NCI-H1975 and Anlotinib-treated Anlotinib-resistant NCI-H1975

Project description:Further to our previous study (E-MTAB-5997), here we performed transcriptome profiling on Anlotinib-resistant NCI-H1975 and Anlotinib-treated Anlotinib-resistant NCI-H1975, and would like to understand the effects of Anlotinib on Anlotinib-resistant NCI-H1975 cell, compare the different transcriptome profiling on NCI-H1975 cells and Anlotinib-resistant NCI-H1975 cells, sought to find the biomarker for explaining Anlotinib resistance.

2019-07-01 | E-MTAB-7068 | biostudies-arrayexpress

Human lung adenocarcinoma NCI-H1975 cells: parental vs cell lines resistant to the EGFR-TK inhibitor CNX-2006

2015-07-01 | GSE53234 | GEO

Gene expression data in the human non-small cell lung cancer cell line NCI-H1975 and osimertinib-resistant OR1 and OR2 cells

Project description:Osimertinib, a third-generation EGFR-TKI, has applied to non-small cell lung cancer harboring activated EGFR mutation with or without T790M. However, the appearance of tumors resistant to osimertinib has been reported. We established and characterized osimertinib-resistant cells derived from NCI-H1975 cells harboring activating EGFR and T790M mutation.

2022-04-28 | GSE201608 | GEO

H1975 MMAB knockdown

Project description:H1975 MMAB knockdown

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Homo sapiens strain:H1975

Project description:H1975 --0915c

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PARP1 and Salmonella

Project description:BACKGROUND & AIMS: The immune system comprises an innate and an adaptive immune response to combat pathogenic agents. The human enteropathogen Salmonella enterica serovar Typhimurium invades the intestinal mucosa and triggers an early innate pro-inflammatory host gene response, which results in diarrheal disease. Several host factors are involved in the acute early response to Salmonella infection. Transcription factors and transcription co-regulators have an especially important function, because they are required for the expression and synthesis of pro-inflammatory cytokines, chemokines and adhesion molecules. A central transcription factor involved in inflammation is NF-ÎºB, which requires the nuclear protein PARP1 as co-factor for the expression of some of its target genes. Here, we investigated the role of PARP1 during Salmonella infection using a mouse model for Salmonella-induced colitis. METHODS: To study enterocolitis by Salmonella Typhimurium, an established mouse model system, which relies on streptomycin-pretreatment prior to Salmonella infection, was employed. Histopathologic signs of inflammation and cecum colonization at various time-points after infection of wild type and PARP1 knockout mice were analyzed. PARP1 expression in the gut mucosa was studied by quantitative RT-PCR, Western blot and immunofluorescence. Gene expression profiles of infected and control infected mice in the wild type or PARP1 knockout background were obtained by whole mouse genome arrays and confirmed by quantitative RT-PCR. 2 genotypes (wildtype, PARP1 knockout), 2 treatments (Salmonella SB300 infection, Salmonella SB161 control infection), 2 time-points (6h, 10h). 2-3 replicates/condition.

2010-05-27 | E-GEOD-19174 | biostudies-arrayexpress

PARP1 expression drives the synergy between trabectedin and PARP1 inhibitors

Project description:Trabectedin is a DNA-damaging agent with a peculiar mechanism of action; it traps the DNA repair machinery leading to DNA single- and double-strand breaks, particularly in BRCA1/2-deficient tumors. We hypothesized that trabectedin-induced DNA damage might activate PARP1 (a DNA-repair machinery key player), and consequently, PARP1 inhibition would perpetuate trabectedin-induced DNA damage. In several tumor histotypes, we demonstrated a different degree of synergism between trabectedin and PARP1 inhibitors (PARP1-Is). Independent of BRCA1/2 status, PARP1 expression dictated the degree of synergism. Namely, silenced PARP1 reduced trabectedin-PARP1-Is synergism, whereas overexpressed PARP1 increased combination efficacy. High-PARP1 expression and specific gene signatures associated with DNA damage response and repair (DDR-R) were predictive of trabectedin+PARP1-I synergy. These findings pave the way for the clinical development of this novel combination therapy, as well as evaluation of PARP1 expression and DDR-R signatures in tumor samples as predictive biomarkers of response

2017-06-12 | GSE77175 | GEO

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