Transcriptome profiling (RNA-seq) of wild type and MYOCD Knockdown in human lung cancer cell line A549.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA529787 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare transcriptome profiling (RNA-seq) of wild type and MYOCD Knockdown in human lung cancer cell line A549. Methods: mRNA profiles of wild type（WT） and Dox inducible MYOCD Knockdown (MYOCD−/−) human lung cancer cell line A549 were generated by deep sequencing, using Illumina GAIIx. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. qRT–PCR validation was performed using TaqMan and SYBR.
2019-03-30 | GSE128918 | GEO
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare transcriptome profiling (RNA-seq) of wild type and MYOCD overexpression in human lung cancer cell line A549. Methods: mRNA profiles of wild type（WT） and MYOCD overexpression (MYOCD) human lung cancer cell line A549 were generated by deep sequencing, using Illumina GAIIx. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. qRT–PCR validation was performed using TaqMan and SYBR.
2019-03-30 | GSE128919 | GEO
Project description:We depleted TIMM13 using short interfering RNA (siRNA) in A549 lung cancer cells, and found that silencing of TIMM13 could significantly inhibit A549 cell proliferation. Thus, we conducted RNA-seq in the A549 cells transduced with either nontargeting siRNA or two distinct TIMM13-specific siRNAs. We observed widespread gene expression change in A549 cells upon TIMM13 knockdown.
2023-06-17 | GSE234780 | GEO
Project description:Transcriptome profiling (RNA-seq) of wild type and MYOCD overexpression in human lung cancer cell line A549.
| PRJNA529786 | ENA
Project description:HSPD1 knockdown was established in A549 cells using an shRNA approach. Secretomes from both shHSPD1-A549 and shControl-A549 cells were collected and subjected to label-free comparative proteome analysis using SWATH-MS.
2024-04-13 | PXD050755 | Pride
Project description:The goals of this study are to compare NGS-derived transcriptome profiling (RNA-seq) in human lung cancer cells. The mRNA profiles of wild-type and C19orf12 knockdown A549 cells were generated by deep sequencing, in triplicate, using Illumina Hiseq 4000. The sequence reads that passed quality filters were analyzed at the transcript isoform level with Burrows–Wheeler Aligner (BWA) and Bowtie2. we sequenced 6 samples of human species using RNA-Seq technology, averagely generating 24,382,600 raw sequencing reads and 24,299,184 clean reads after filtering low quality. We identified 20826 transcripts in the of WT and C19orf12 knockdown A549 samples with BWA workflow. Approximately 2% of the transcripts showed differential expression between the WT and C19orf12 knockdown A549 cells, p value <0.05. Altered expression of 21 genes was confirmed with qRT–PCR, demonstrating the high degree of sensitivity of the RNA-seq method. We conclude that RNA-seq based transcriptome characterization would providing clues for better understanding of gene function.
2021-06-30 | GSE133661 | GEO
Project description:Asthma is characterized by intermittent inflammation of the airways, airflow limitation and wheeze. The ORMDL3 locus on chromosome 17q21 confers the major genetic susceptibility to childhood asthma. Although sphingolipids are important in immune signalling, the mechanisms of action of ORMDL3 on airway inflammation are incompletely understood. We used Affymetrix Human Gene 1.1 ST microarrays to detail the global effects of siRNA-mediated ORMDL3 knockdown during the time course of IL1B-induced inflammation in the A549 Human Lung Epithelial cell line.
2018-11-21 | GSE92484 | GEO
Project description:Enriched p53 signalling after MILIP knockdown was validated by RNA-seq; A c-myc reponsive lncRNA MILIP is commonly upregulated in diverse cancer types. RNA-seq analysis of A549 cells following MILIP knockdown revealed that p53 signalling was the mostly enriched gene pathway, suggesting c-Myc may inactivate p53 through MILIP in cancer.
2020-08-19 | GSE141886 | GEO
Project description:Aberrant mucin-type O-glycosylation affects many cellular properties and is associated with many cancers. N-acetylgalactosaminyltransferase 10 (GALNT10) is a GalNAc-transferase that initiates protein O-glycosylation. The aim of this study was to explore the role of GALNT10 in lung adenocarcinoma. Immunohistochemistry was performed to study the expression of GALNT10 in an lung adenocarcinoma tissue microarray. We found that GALNT10 is frequently down-regulated in lung adenocarcinoma tissues and is associated with pathological classification and TNM stage. Additionally, we demonstrated that knockdown of GALNT10 with small interference (si) RNA promoted cell proliferation, cell colony formation and cell invasion capacity in A549 cells by using CCK8 assay, flow cytometry, cell colony formation, and transwell invasion assay.Moreover, whole genome microarray analysis showed that 287 genes were up-regulated and 137 were down-regulated in A549 cells upon GALNT10 knockdown. Functional enrichment analysis reveal that GALNT10 knockdown in A549 cells leads to differential gene expression in pathways, including TNF signaling pathway. These findings suggest that down-regulation of GALNT10 plays an important role in the cell proliferation and invasive behavior of lung adenocarcinoma via modifying O-glycosylation and activity of TNF pathway. In addition, we suggest that GALNT10 may be a tumor suppressor gene in lung adenocarcinoma and that targeting GALNT10 could be a promising approach for lung adenocarcinoma therapy.
2019-03-27 | GSE128887 | GEO
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
2015-05-15 | E-GEOD-68869 | biostudies-arrayexpress