Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Comparison of gene expression in xenograft tissue stably expressing ShRNA KDM1A

ABSTRACT: The purpose of this study was to chacterise the effect of KDM1A knocking down on genome-wide gene expression in human NSCLC cells in vivo. Affymetrix human transcriptome array 2.0 was used to profile the transcriptome of xenograft tumors derived from PC9 cells stably expressing either ShRNA KDM1A or ShRNA control. These cells were subcutanously injected into the right axillary of the mouse, and allowd to grow for 5 weeks to form xenograft tumors. Although KDM1A is up-regulated in NSCLC, but key genes and pathways regulated by KDM1A was not well-understood in NSCLC. Using this approach, we have shown that KDM1A repressed or activated a distinctive set of pathways and key target genes in vivo. This first comprehesive study of transciptome profile upon KDM1A koncking-down in vivo highlights the distinctive pathways regulated by KDM1A during NSCLC tumorigenesis, and it will help to identify new therapeutic targets for NSCLC treatment. Xenograft tumors derived from two cell lines: PC9 cells stably expressing ShRNA KDM1A or ShRNA control. We extracted total RNA from 3 independent xenograft tumors per cell line.

ORGANISM(S): Homo sapiens

SUBMITTER: FAN ZHANG

PROVIDER: E-GEOD-71358 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Comparison of gene expression in xenograft tissue stably expressing ShRNA KDM1A

Project description:The purpose of this study was to chacterise the effect of KDM1A knocking down on genome-wide gene expression in human NSCLC cells in vivo. Affymetrix human transcriptome array 2.0 was used to profile the transcriptome of xenograft tumors derived from PC9 cells stably expressing either ShRNA KDM1A or ShRNA control. These cells were subcutanously injected into the right axillary of the mouse, and allowd to grow for 5 weeks to form xenograft tumors. Although KDM1A is up-regulated in NSCLC, but key genes and pathways regulated by KDM1A was not well-understood in NSCLC. Using this approach, we have shown that KDM1A repressed or activated a distinctive set of pathways and key target genes in vivo. This first comprehesive study of transciptome profile upon KDM1A koncking-down in vivo highlights the distinctive pathways regulated by KDM1A during NSCLC tumorigenesis, and it will help to identify new therapeutic targets for NSCLC treatment.

2016-07-27 | GSE71358 | GEO

Homo sapiens

Project description:Comparison of gene expression in xenograft tissue stably expressing ShRNA KDM1A

| PRJNA291021 | ENA

Single cell RNA sequencing analysis of freshly resected PC9 cell line-derived tumor xenografts

Project description:The non-small cell lung carcinoma (NSCLC) PC9 cell line is an established preclinical model for tyrosine kinase inhibitors. Using PC9 cells, we generated EGFR-mutant lung cancer xenografts to study the differences in response between individual cells and cell populations. We performed treatment of PC9 xenograft tumors with the combination of osimertinib and crizotinib as well as single drugs, followed by Drop-seq. The addition of crizotinib was guided by our previous data in PC9 grown in cell culture that identified an erlotinib-resistant drug population sensitive to crizotinib. The results of the xenograft study show that combination treatment targets specific osimertinib-tolerant cell populations but leaves a subset of the population that is tolerant to the combo. Each cell subpopulation is characterized by specific molecular signatures. The results of our study help to address emerging drug resistance that limits clinical usefulness of targeted strategies, particularly in NSCLC.

2020-12-19 | GSE160244 | GEO

Phosphoproteomics of in vivo resistance to EGFR-targeted therapy in lung cancer cells

Project description:Mass spectrometry-based quantitative proteomics profiling of in vivo signaling changes in 41 therapy resistant (osimertinib or EGFR/Met bispecific antibody treament) tumors from four xenograft NSCLC models.

2017-08-28 | PXD006114 | Pride

Transcriptome analysis of PC9 cells with gefitinib or/and hypoxia treatment and comparison with gefitinib resistant PC9 cells and ALDH positive PC9 cells

Project description:Inevitable gefitinib resistance and relapse of the disease was the biggest hurdle to NSCLC treatment. Importantly, the role of hypoxia in solid tumor tissues in vivo in gefitinib acquired resistance and its relationship to lung cancer stem cells (LCSCs) has not been fully elucidated. Here, the PC9 cells were treated with short term gefitinib or/and hypoxia, also, PC9 gefitnib resistant (PC9-GR) cell line was established and ALDH positive PC9 cells were sorted by FACs. Transcriptome analysis among those PC9 cell groups revealed the important role of hypoxia in gefitinib acquired resistance and signaling transduction change, which may critical for NSCLC disease progression and recurrence.

2017-10-31 | GSE69599 | GEO

DNA Methylome Analysis of Human Cancer Cells with STELLA Protein Overexpression and the Xenograft Tumor Tissues from the Mice Treated by the Indicated LNP Formulations

Project description:Genome-wide DNA methylation profiling of non-small cell lung cancer (NSCLC) cell line A549 and breast cancer cell line MDA-MB-231 stably expressing hSTELLA and mSTELLA, as well as the HCT116 xenograft tumor tissues from the mice treated by the indicated LNP formulations. The Infinium MethylationEPIC v2.0 array was used to obtain DNA methylation profiles across more than 935,000 CpGs in 15 samples. Samples included 3 stable NSCLC cells and 3 stable breast cancer cells expressing the STELLA orthologs, and 9 xenograft tumors from the mice with the indicated treatments.

2024-07-28 | GSE273176 | GEO

PKCÎ´ regulates the transformed growth of K-ras dependent lung cancer cells through regulation of integrin Î±VÎ²3 expression

Project description:To explore how PKCÎ´ regulates tumorigenesis, we performed mRNA expression analysis of four KRAS mutant NSCLC cell lines that stably express scrambled shRNA or PKCÎ´ targeted shRNA Four human lung cancer cell lines (A549, H441, H460 and H2009) with scrambled and PKC-delta knock down (shRNA), in triplicate.

2016-09-01 | E-GEOD-72788 | biostudies-arrayexpress

KDM1A confers invasive and metastatic attributes in lung adenocarcinoma by modulating a non-canonical Integrin ß3-KRAS signaling pathway

Project description:KRAS mutations occur in approximately 25% of non-small cell lung cancer (NSCLC). They account for the therapy resistance to EGFR inhibitors and are suggested to be difficult to target by specific drugs. Therefore, new therapies for KRAS mutant NSCLC are urgently needed. The histone H3K4 and H3K9 di/mono-demethylase KDM1A is a key epigenetic writer, aberrantly upregulated in many cancer types, including NSCLC. In order to understand the functional role of KDM1A in the progression of lung adenocarcinoma, KDM1A expression profiles were analysed in tissue microarrays (TMAs) including 182 lung adenocarcinoma. KDM1A expression correlated with high grade and metastasized tumor. To investigate the impact of KDM1A in lung adenocarcinoma development, we used the KRAS mutated A549 cell line to establish a shRNA-mediated stable KDM1A knockdown cell clone. Unexpectedly, KDM1A knockdown had only a slight effect on retardation of cell growth. However, cell invasion and self-renewal capability was significantly decreased by KDM1A inhibition. KDM1A knockdown in A549 cell resulted in a dramatic change in the transcriptome profile as determined by RNA-Seq. Interestingly, genes involved in the KRAS signature and lung epithelial marker genes were significantly affected upon KDM1A knockdown. Ingenuity pathway analysis also suggested that the alternative integrin β3-KRAS signaling axis, which is involved in stem cell like properties, is abrogated upon KDM1A knockdown. Indeed, Integrin β3 and its non-canonical ligand galectin-3 were strongly downregulated and their downstream NF-κB activity was decreased upon KDM1A knockdown. Finally, correlation of KDM1A to the Integrin β3 level was validated in TMAs.

2017-03-13 | GSE86874 | GEO

PKCδ regulates the transformed growth of K-ras dependent lung cancer cells through regulation of integrin αVβ3 expression

Project description:To explore how PKCδ regulates tumorigenesis, we performed mRNA expression analysis of four KRAS mutant NSCLC cell lines that stably express scrambled shRNA or PKCδ targeted shRNA

2016-09-01 | GSE72788 | GEO

Overcoming TKI resistance in a lung xenograft model

Project description:Bulk RNA-Seq of PC9 xenograft tumors in different stages of response and resistance to Erlotinib treatment. A combination treatment is proposed in order to overcome Erlotinib drug resistance.

2020-11-17 | GSE161584 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data