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Expression data from A549 human lung adenocarcinoma cells with and without knockdown against CNOT3

ABSTRACT: Expression data from A549 human lung adenocarcinoma cells with and without knockdown against CNOT3

PROVIDER: PRJNA472252 | ENA |

REPOSITORIES: ENA

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Expression data from A549 human lung adenocarcinoma cells with and without knockdown against CNOT3

Project description:The physiological importance of mRNA degradation through the CCR4-NOT deadenylase has recently been highlighted. For example, mutation in CNOT3, a gene coding for sCNOT3 subunit of the CCR4-NOT complex, is found to be associated with T-cell acute lymphoblastic leukemia, T-ALL, though its contribution to other cancers has not been reported. To identify the taget mRNAs of CNOT3 in human non-small cell lung cancer (NSCLC), we performed the microarray analysis using A549 cells with and without knockdown against CNOT3.

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Gene expression profile of Cnot3(+/+) & Cnot3 (∆/∆) pro-B cells

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Lung Adenocarcinoma (A549) Immunopeptidomics

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.

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Lung Adenocarcinoma (A549) Immunopeptidomics

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Transcription profiling of human lung adenocarcinoma derived cell line A549 treated with dexamethasone

Project description:Effect of dexamethasone on gene expression in lung adenocarcinoma derived cell line A549

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Transcription profiling of human lung adenocarcinoma derived cell line A549 treated with testosterone

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Knockdown of CUL3 and PTEN in A549 lung adenocarcinoma cells

Project description:Non-small cell lung cancers (NSCLCs) harbor thousands of passenger events that hide genetic drivers. Even highly recurrent events in NSCLC, such as mutations in PTEN, EGFR, KRAS, and ALK, are only detected in, at most, 30% of patients. Thus, many unidentified low-penetrant events are causing a significant portion of lung cancers. To detect low-penetrance drivers of NSCLC a forward genetic screen was performed in mice using the Sleeping Beauty (SB) DNA transposon as a random mutagen to generate lung tumors in a Pten deficient background. SB mutations coupled with Pten deficiency were sufficient to produce lung tumors in 29% of mice. Pten deficiency alone, without SB mutations, resulted in lung tumors in 11% of mice, while the rate in control mice was ~3%. In addition, thyroid cancer and other carcinomas as well as the presence of bronchiolar and alveolar epithelialization in mice deficient for Pten were also identified. Analysis of common transposon insertion sites identified 76 candidate cancer driver genes. These genes are frequently dysregulated in human lung cancers and implicate several signaling pathways. Cullin3 (Cul3), a member of an ubiquitin ligase complex that plays a role in the oxidative stress response pathway, was identified in the screen and evidence demonstrates that Cul3 functions as a tumor suppressor HumanHT-12 v4 Expression BeadChip Kit for human A549 lung adenocarcinoma cells with CUL3, PTEN, CUL3 and PTEN or no knockdown. A549 cells were stably transfected under Puromycin or Hygromycin selection to knockdown PTEN (SA Biosystems) or CUL3 (Open Biosystems) shRNAs. RNA was extracted in triplicate from each condition and used for microarray

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Pulsed cisplatin treatment of A549 lung adenocarcinoma cells

Project description:A549 lung adenocarcinoma cells were pulsed for 2h with cisplatin and allowed to recover for 3 days. Cells were then FACS sorted based on size and enriched populations analysed for RNAseq.

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expression data from human lung adenocarcinoma cells A549

Project description:GMDS is important for human lung adenocarcinoma progression, detailed molecular mechanisms remain elusive. We used microarray to detail the global gene expression changes in A549 cells with GMDS knockdown as compared to control cells

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