Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA357552 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Immunoprecipitation of EGFR from irradiated A549 (ATCC CCL185) cells was performed in order to characterize bound mRNA species with the help of microarray analysis As control experiment, immunoprecipitation was also performed with IgG
2017-12-21 | GSE92428 | GEO
Project description:The epidermal growth factor receptor (EGFR) is frequently overexpressed in cancer and is an important therapeutic target. Aberrant expression and function of microRNAs has been associated with tumorigenesis. Bioinformatic predictions suggest that the human EGFR mRNA 3’-untranslated region contains three microRNA-7 (miR-7) target sites, which are not conserved across mammals. We found that miR-7 down-regulates EGFR mRNA and protein expression in cancer cell lines (lung, breast, and glioblastoma) via two of the three sites, inducing cell cycle arrest and cell death. Because miR-7 was shown to decrease EGFR mRNA expression, we used microarray analysis to identify additional mRNA targets of miR-7. These included Raf1 and multiple other genes involved in EGFR signaling and tumorigenesis. Furthermore, miR-7 attenuated activation of protein kinase B (Akt) and extracellular signal-regulated kinase 1/2 (ERK1/2), two critical effectors of EGFR signaling, in different cancer cell lines. These data establish an important role for miR-7 in controlling mRNA expression and indicate that miR-7 has the ability to coordinately regulate EGFR signaling in multiple human cancer cell types. Four samples are analysed: two biological replicates of A549 cells treated with miR-7 precursor and two biological replicates of A549 cells treated with miR-NC negative control precursor.
2009-01-23 | E-GEOD-14507 | biostudies-arrayexpress
Project description:In this study, we explored the role of FXR in the response to ionizing radiation (IR) in A549 human lung cancer cells. FXR was stably knocked down in A549 cells using shRNA, and four experimental groups were established: control A549 cells (non-irradiated), control A549 cells (irradiated), FXR knockdown A549 cells (non-irradiated), and FXR knockdown A549 cells (irradiated). RNA sequencing (RNA-seq) was performed to identify gene expression changes associated with FXR knockdown and irradiation. This dataset provides insights into the molecular mechanisms by which FXR influences the cellular response to radiation and its potential impact on cancer therapy.
2024-10-31 | GSE278872 | GEO
Project description:In this study, we explored the role of TRIM22 in the response to ionizing radiation (IR) in A549 human lung cancer cells. TRIM22 was stably knocked down in A549 cells using shRNA, and four experimental groups were established: control A549 cells (non-irradiated), control A549 cells (irradiated), TRIM22 knockdown A549 cells (non-irradiated), and TRIM22 knockdown A549 cells (irradiated). RNA sequencing (RNA-seq) was performed to identify gene expression changes associated with TRIM22 knockdown and irradiation. This dataset provides insights into the molecular mechanisms by which TRIM22 influences the cellular response to radiation and its potential impact on cancer therapy.
2025-01-01 | GSE277805 | GEO
Project description:<p>Non-small cell lung cancer is a malignant tumor with high morbidity and mortality worldwide. Eleutherococcus senticosus can induce apoptosis in non-small cell lung cancer cells, but the mechanism remains unclear. This study aimed to elucidate the role of Eleutherococcus senticosus in inducing apoptosis in non-small cell lung cancer cells and analyze its potential active constituents, targets and molecular mechanisms. The results of network pharmacology analysis showed that Eleutherococcus senticosus contained 49 active ingredients that induced apoptosis in non-small cell lung cancer cells, and these components could act on 66 apoptosis-related targets. Compared to the control group, Eleutherococcus senticosus significantly increased apoptosis in A549 cells with increasing concentration (p < 0.05). The results of transcriptome and metabolomic analyses showed that Eleutherococcus senticosus significantly changed 5836 genes and 418 metabolites in A549 cells (p < 0.05), with the most significant changes in 18 genes and 34 metabolites related to apoptosis. qRT-PCR and Western blot results showed that, after Eleutherococcus senticosus treatment, the mRNA and protein expression of EGFR, MAPK3, and ICAM1 significantly increased, while CTSK decreased (p < 0.01 or p < 0.001). Correlation analysis and molecular docking results indicated that calycanthoside and oleanolic acid can directly modify the expression levels of the transcription factors POU2F3, FOXS1 and TGIF2LY or indirectly influence the binding affinity of these transcription factors to the promoters of key target genes, ultimately leading to the activation of EGFR, MAPK3, ICAM1 and CTSK, which triggers apoptosis in non-small cell lung cancer cells.</p>
2025-05-12 | MTBLS10545 | MetaboLights
Project description:mRNA Expression data from sodium butyrate or sodium phenylbutyrate treated A549 cells
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Project description:Expression data for EGFR TKI resistant EGFR-mutated Cells
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Project description:We have employed microarray expression profiling as a discovery platform to identify microRNAs induced by radiation. Human A549 lung cancer cells were irradiated (2Gy/day for consistent 3days) and miRNA signature was identified that distinguished between control and radiation treated samples.Irradiated and un-irradiated A549 cells were harvested after 48 hr of treatment and microarray analysis was performed. Expression of five miRNAs (miR-30a, miR-30b, miR-30c, miR-30d, and miR-30d) from this signature was quantified in the same RNA samples by real-time PCR, confirming variability between control and radiation treated A549 cells.
2017-07-11 | GSE101085 | GEO
Project description:The receptor tyrosine kinase (RTK) EGFR is overexpressed and mutated in NSCLC. These mutations can be targeted by RTK inhibitors (TKIs), such as erlotinib. Chromatin-modifying agents offer a novel therapy approach by sensitizing tumor cells to TKIs. The NSCLC cell lines HCC827 (EGFR mutant, adenocarcinoma), A549 (EGFR wt, adenocarcinoma) and NCI-H460 (EGFR wt, large cell carcinoma) were analyzed by SNP6.0 array. Changes in proliferation were quantified by WST-1 assay, apoptosis by Annexin V/7-AAD flow cytometry and histone marks (acH3, H3K4me1,-2,-3) by immunoblotting. Expectedly, the EGFR wt cell lines A549 and NCI-H460 were insensitive to the growth-inhibiting effect of single-agent erlotinib (IC50 70-100µM), compared to HCC827 (IC50 <0.02μM). Treatment with panobinostat diminished growth to <50% in both EGFR wt and <30% in HCC827 cells. The combination of both drugs significantly reduced proliferation by ≥70% in A549, >95% in HCC827, but not further in NCI-H460. Panobinostat alone induced differentiation and expression of p21WAF1/CIP1 and p53 in all three cell lines, with almost no further increase when combined with erlotinib. In contrast, combination treatment additively decreased pERK, pAKT and pEGFR in A549, and synergistically induced acH3 in both adenocarcinoma lines. Surprisingly, we also saw an induction of H3K4 methylation marks in all three cell lines. In conclusion, panobinostat synergistically sensitized lung adenocarcinoma cells to the antiproliferative effects of erlotinib. Since single-agent erlotinib has only modest clinical effects in adenocarcinoma EGFR wt patients, combination therapy with an HDACi might offer a promising therapy approach to extend this activity. Copy-number analysis of three NSCLC cell lines HCC827, A549 and NCI-H460 (in unicates) was performed according to protocol by Affymetrix Genome-Wide Human SNP-Array 6.0.
2014-12-03 | E-GEOD-63784 | biostudies-arrayexpress
Project description:Expression data from human unbilical endothelial cells (HUVEC) irradiated with X-ray
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