Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Warburg effect enhanced by AKR1B10 promotes acquired resistance to pemetrexed in lung cancer-derived brain metastasis

ABSTRACT: To investigate the function of AKR1B10 in the lung cancer brain metastasis cells, we established PC9-BrM3 cells in which AKR1B10 has been knocked down by shRNA.

ORGANISM(S): Homo sapiens

PROVIDER: GSE211215 | GEO | 2023/08/23

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

CD146 as a potent target for anti-vascular therapies in lung cancer brain metastasis

Project description:To investigate the function of CD146 in the lung cancer brain metastasis cells, we established PC9-BrM3 cells in which CD146 has been knocked down by shRNA.

2023-12-31 | GSE248935 | GEO

Reactive astrocytes promote tumor progression via up-regulating tumor PCDH1 expression in lung cancer brain metastasis

Project description:To investigate the function of PCDH1 in the lung cancer brain metastasis cells, we established PC9-BrM3 cells in which PCDH1 has been knocked down by shRNA.

2024-02-05 | GSE244170 | GEO

Warburg effect enhanced by AKR1B10 promotes acquired resistance to pemetrexed in lung cancer-derived brain metastasis

Project description:Warburg effect enhanced by AKR1B10 promotes acquired resistance to pemetrexed in lung cancer-derived brain metastasis

2023-07-10 | PXD043632 | iProX

Comparative transcriptome of cancer cells with enhanced brain tropism

Project description:Comparative transcriptome analysis of WM266.4 versus WM266.4-BrM3 human melanoma cells and PC9 versus PC9-BrM4 human lung cancer cells

2020-05-15 | GSE150560 | GEO

Characterizing an HSF1-dependent transcriptional program in metastatic lung adenocarcinoma

Project description:The purpose of this study was to identify gene targets differentially regulated by shRNA-mediated knockdown of the HSF1 transcription factor in the brain-metastatic lung adenocarcinoma cell line PC9-BrM3.

2021-01-06 | GSE149246 | GEO

The effect on gene expression by p53 family members and the knockdown of AKR1B10

2013-10-31 | GSE47096 | GEO

Identification of PARP1 target genes using microarray

Project description:Purpose:To indentify downtream effectors of PARP1, we performed microarray profiling in non-targeting or PARP1 targeting shRNA-expressing H2030-BrM3. Results: we identifed 15 genes whose expression were decreased upon depletion of PARP1 in H2030-BrM3 cells at least by under 1.3-fold.

2015-10-07 | GSE73735 | GEO

The effect on gene expression by p53 family members and the knockdown of AKR1B10

Project description:To evaluate the effect on gene expression by p53 family members and AKR1B10, we overexpressed p53 family members in H1299 cells or knocked down AKR1B10 in HCT116 cells and evaluated the gene expression by microarray analysis. Gene expression was measured in H1299 cells infected with adenovirus expressing p53, p63g and p73b, and in HCT116 cells transfected with siRNAs targeting AKR1B10 and then treated with adriamycin.

2013-10-31 | E-GEOD-47096 | biostudies-arrayexpress

IL-8 Confers Acquired Resistance to EGFR Inhibitors through Regulating Stem Cell-like Properties in Lung Cancer

Project description:Previous study has demonstrated that PC9/gef cells are resistant to gefitinib-induced aspoptosis. To investigate the regulators contributed to gefitinib resistance in lung cancer, we analyzed the gene expression profiles between PC9 and PC9/gef cells. Our results showed that IL-8 contributes to gefitinib resistance and cancer stemness. In contrast, IL-8 knockdown decreased stem-like characteristics and increased gefitinib-induced apoptosis in PC9/gef cells. RNAs extracted from gefitinib-sensitive PC9 cells and gefitinib-resistant PC9/gef cells were hybridized on Affymetrix microarrays. We tried to compare the differential gene expression profiles between PC9 and PC9/gef cells to identify the possible regulators in gefitinib resistance.

2015-08-12 | E-GEOD-60189 | biostudies-arrayexpress

Proteomic reveals reasons for acquired drug resistance in lung cancer derived brain metastasis based on a newly established multi-organ microfluidic chip model

Project description:Anti-tumor drugs can effectively shrink the lesions of primary lung cancer; however, it has limited therapeutic effect on patients with brain metastasis (BM). A BM preclinical model based on a multi-organ microfluidic chip has been established proficiently in our previous work. In this study, the BM subpopulation (PC9-Br) derived from the parental PC9 cell line was isolated from the chip model and found to develop obvious resistance to antineoplastic drugs including chemotherapeutic agents (cisplatin, carboplatin, pemetrexed) and tyrosine kinase inhibitors (TKIs) which target epidermal growth factor receptor (EGFR); this suggested that the acquisition of drug-resistance by brain metastatic cells was attributable to the intrinsic changes in PC9-Br. Hence, we performed proteomic and revealed a greatly altered spectrum of BM protein expression compared with primary lung cancer cells.

2021-09-09 | PXD021760 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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