E-GEOD-18182
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA123513PRJNA123489PRJNA119645PRJNA173992PRJNA174034PRJNA174033PRJNA173068
PROVIDER: E-GEOD-18182 | ExpressionAtlas | 2015-08-07
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE18182: Expression profile of lung adenocarcinoma, A549 cells following targeted depletion of non metastatic 2 (NME2/NM23 H2) GSE18284: Genomic binding sites of non-metastatic 2 (NME2) across promoters in lung cancer A549 cells Refer to individual Series
2011-02-08 | E-GEOD-18285 | biostudies-arrayexpress
Project description:Expression profile of lung adenocarcinoma, A549 cells following targeted depletion of non metastatic 2 (NME2/NM23 H2)
| PRJNA123489 | ENA
Project description:Expression profile of lung adenocarcinoma, A549 cells following induction of non metastatic 2 (NME2/NM23 H2)
| PRJNA173068 | ENA
Project description:Background: Lung cancer, particularly lung adenocarcinoma, remains one of the most lethal malignancies globally. Identifying aberrant molecular pathways and potential therapeutic targets is pivotal for improving patient outcomes. This study focused on the role of GSE1 (genetic suppressor element 1) in lung adenocarcinoma, elucidating its interaction mechanisms and downstream effects. Objectives: 1. Determine the expression levels of GSE1 in lung adenocarcinoma tissues and its implication on cancer cell behaviors. 2. Investigate the effects of GSE1 depletion on the proliferation and migration capabilities of A549 and H1299 lung adenocarcinoma cell lines. 3. Elucidate the potential cellular partners of GSE1, with a particular focus on its interaction with histone deacetylase 1 (HDAC1) and the broader BRAF-HDAC complex (BHC). 4. Analyze the transcriptomic changes following GSE1-knockdown in A549 cells to pinpoint its broad molecular influence. 5. Examine the possible cooperative role of GSE1 and HDAC1 in modulating the expression of significant genes, especially the tumor suppressor gene KLF6. Methods: GSE1 expression was assessed in lung adenocarcinoma tissues and correlated with cell behaviors. The effects of GSE1 depletion were studied in A549 and H1299 cells. Immunoprecipitation assays were utilized to confirm GSE1's interactions. Transcriptomic analysis identified differentially expressed genes post-GSE1-knockdown, with a focus on genes harboring HDAC1 binding sites. The relationship between GSE1 and KLF6 expression was verified using RT-qPCR and western blotting. Results: GSE1 was found to be upregulated in lung adenocarcinoma. Its depletion inhibited proliferation and migration in both A549 and H1299 cells. GSE1 was demonstrated to interact with HDAC1 and other BHC components. Following GSE1-knockdown, 207 genes were upregulated and 159 were downregulated, with 140 genes showcasing HDAC1 binding sites. Among these genes, GSE1 was revealed to inhibit the transcription of the tumor suppressor gene KLF6. Conclusion: GSE1 plays a central role in promoting non-small cell lung cancer progression, potentially through its cooperation with HDAC1. This interaction appears to downregulate KLF6 expression, highlighting a novel molecular pathway that can be targeted for therapeutic interventions in lung adenocarcinoma.
2023-09-10 | GSE242323 | GEO
Project description:Alterations in cellular antigen processing and presenting machinery has gained increased interest as a hallmark of cancer-related inflammation. Growing evidence suggest that proteasome composition and immunoproteasome expression can influence antigen processing. By performing immunopeptidomics on A549 lung adenocarcinoma cell line following depletion of proteasome regulator PSME4 we identified alterations in the antigenic landscape resulting from changes in proteasome processing.
2023-03-30 | PXD028364 | Pride
Project description:Alterations in cellular antigen processing and presenting machinery has gained increased interest as a hallmark of cancer-related inflammation. Growing evidence suggest that proteasome composition and immunoproteasome expression can influence antigen processing. By performing immunopeptidomics on A549 lung adenocarcinoma cell line following depletion of proteasome regulator PSME4 we identified alterations in the antigenic landscape resulting from changes in proteasome processing.
2023-03-30 | PXD037365 | Pride
Project description:To determine the signaling networks that are dysregulated in cisplatin-resistant non-small cell lung cancer, noncoding RNA expression data were obtained from, and compared between, the lung adenocarcinoma cell line, A549, and its cisplatin-resistant derivative, A549/CDDP. Noncoding RNA expression data from a cisplatin-sensitive lung adenocarcinoma cancer cell line (A549) were collected and compared to noncoding RNA expression data from a cisplatin-resistant cell line (A549/CDDP). 3 independent experiments were completed for both the sensitive and resistant cell lines.
2013-01-15 | E-GEOD-43249 | biostudies-arrayexpress
Project description:To determine the signaling networks that are dysregulated in cisplatin-resistant non-small cell lung cancer, noncoding RNA expression data were obtained from, and compared between, the lung adenocarcinoma cell line, A549, and its cisplatin-resistant derivative, A549/CDDP. Noncoding RNA expression data from a cisplatin-sensitive lung adenocarcinoma cancer cell line (A549) were collected and compared to noncoding RNA expression data from a cisplatin-resistant cell line (A549/CDDP). 3 independent experiments were completed for both the sensitive and resistant cell lines.
2013-01-15 | E-GEOD-43493 | biostudies-arrayexpress
Project description:Lung cancer is the leading cause of cancer death both in men and women. Tumor heterogeneity is an impediment to targeted treatment of all cancers, including lung cancer. Here, we sought to characterize changes in tumor proteome and phosphoproteome by longitudinal, prospective collection of tumor tissue of an exceptional responder lung adenocarcinoma patient who survived with metastatic lung adenocarcinoma for more than seven years with HER2-directed therapy in combination with chemotherapy. We employed “Super-SILAC” and TMT labeling strategies to quantify the proteome and phosphoproteome of a lung metastatic site and ten different metastatic progressive lymph nodes collected across a span of seven years, including five lymph nodes procured at autopsy. We identified specific signaling networks enriched in lung compared to the lymph node metastatic sites. We correlated the changes in protein abundance with changes in copy number alteration (CNA) and transcript expression. To further interrogate the mass spectrometry data, patient-specific database was built incorporating all the somatic variants identified by whole genome sequencing (WGS) of genomic DNA from the lung, one lymph node metastatic site and blood. An extensive validation pipeline was built for confirmation of variant peptides. We validated 360 spectra corresponding to 55 germline and 6 somatic variant peptides. Targeted MRM assays demonstrated expression of two novel variant somatic peptides, CDK12 G879V and FASN-R1439Q, with expression in lung and lymph node metastatic sites, respectively. CDK12 G879V mutation likely results in a nonfunctional kinase and knockdown of CDK12 in lung adenocarcinoma cells increased chemotherapy sensitivity, explaining the complete resolution of the lung metastatic sites in this patient.
2019-01-07 | PXD010779 | Pride
Project description:To determine the signaling networks that are dysregulated in cisplatin-resistant non-small cell lung cancer, noncoding RNA expression data were obtained from, and compared between, the lung adenocarcinoma cell line, A549, and its cisplatin-resistant derivative, A549/CDDP.
2013-01-15 | GSE43493 | GEO