Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

14 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MiRNA expression of lung cancer cells A549 and cisplatin (DDP) resistant lung cancer cells A549/DDP

ABSTRACT: To investigate the difference of miRNA expression between lung cancer cell A549 and its DDP-resistant cell strain A549/DDP, we have employed miRNA microarray expression to discover the difference expression of miRNAs of A549 cells and A549/DDP. We conducted RT-qPCR to examine the expression levels of top differential expressed miRNAs, namely, miR-197-5p, miR-4443, miR-642a-3p, miR-27b-3p and miR-100-5p, confirming low variability between two methods. The A549/DDP was established from A549 in our laboratory, by exposing A549 to gradually increasing DDP concentrations, until the final concentration at 1Î¼g/ml. To avoid the influence of drug to the A549/DDP cells, they were cultured in a drug-free medium for at least two weeks before gene expression analysis. miRNA expression of A549 and A549/DDP was then analzyed.

ORGANISM(S): Homo sapiens

SUBMITTER: Jifeng Feng

PROVIDER: E-GEOD-85603 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

miRNA expression of exosomes derived from lung cancer cells A549 and cisplatin (DDP) resistant lung cancer cells A549/DDP

Project description:To investigate the difference of miRNA expression in exosomes derived from A549 cells and its DDP-resistant cell strain A549/DDP, we have employed miRNA microarray expression to discover the difference expression of miRNAs in exosomes derived from A549 and A549/DDP. We conducted RT-qPCR to examine the expression levels of top differential expressed miRNAs, namely, miR-197-5p, miR-4443, miR-642a-3p, miR-27b-3p and miR-100-5p, confirming low variability between two methods. The A549/DDP was established from A549 in our laboratory, by exposing A549 to gradually increasing DDP concentrations, until the final concentration at 1Î¼g/ml. To avoid the influence of drug to the A549/DDP cells, they were cultured in a drug-free medium for at least two weeks before gene expression analysis. After being incubated for 48-72h, the culture medium of cells was harvested. Exosomes were isolated by ultracentrifugation. And miRNA expression of exosomes derived from A549 and A549/DDP was then analzyed.

2016-08-16 | E-GEOD-85604 | biostudies-arrayexpress

miRNA expression of lung cancer cells A549 and cisplatin (DDP) resistant lung cancer cells A549/DDP

Project description:To investigate the difference of miRNA expression between lung cancer cell A549 and its DDP-resistant cell strain A549/DDP, we have employed miRNA microarray expression to discover the difference expression of miRNAs of A549 cells and A549/DDP. We conducted RT-qPCR to examine the expression levels of top differential expressed miRNAs, namely, miR-197-5p, miR-4443, miR-642a-3p, miR-27b-3p and miR-100-5p, confirming low variability between two methods.

2016-08-16 | GSE85603 | GEO

miRNA expression of exosomes derived from lung cancer cells A549 and cisplatin (DDP) resistant lung cancer cells A549/DDP

2016-08-16 | GSE85604 | GEO

Genome-wide analysis of miR-552-3p- and miR-608-mediated gene silencing in A549 lung cancer cells

Project description:Analysis of changes in gene expression after transfection with miR-552-3p or miR-608 mimic in A549 cells Total RNA was obtained from A549 cells transfected with miR-552-3p or miR-608 or negative control mimic, and gene expression was compared using microarrays.

2015-12-15 | E-GEOD-62723 | biostudies-arrayexpress

Genome-wide analysis of miR-509-3p-mediated gene silencing in A549 lung cancer cells

Project description:Analysis of changes in gene expression after transfection with miR-509-3p mimic in A549 cells Total RNA was obtained from A549 cells transfected with miR-509-3p and negative control mimics, and gene expression was compared using microarrays.

2014-05-31 | E-GEOD-47522 | biostudies-arrayexpress

Integration of metabolomics and transcriptomics to reveal metabolic characteristics and key targets associated with cisplatin resistance in non-small cell lung cancer

Project description:Continuous exposure to cisplatin can induce drug resistance to limit efficacy, however, the underlying mechanisms correlated to cisplatin resistance are still unclear. Drug-sensitive A549 cells and cisplatin-resistant A549/DDP cells were used to explore the potential metabolic pathways and key targets associated with cisplatin resistance by integrating untargeted metabolomics with transcriptomics. The results of comprehensive analyses showed that 19 metabolites were significantly changed in A549/DDP vs A549 cells, and some pathways had a close relationship with cisplatin resistance, such as the biosynthesis of aminoacyl-tRNA, glycerophospholipid metabolism, and glutathione metabolism. Moreover, transcriptomics analysis showed glutathione metabolism was also obviously affected in A549/DDP, which indicated that glutathione metabolism played an import role in the process of drug resistance. Meanwhile, transcriptomics analysis suggested the four enzymes related to glutathione metabolism - CD13, GPX4, RRM2B, and OPLAH - as potential targets of cisplatin resistance in NSCLC. Further studies identified the over-expressions of these four enzymes in A549/DDP. The elucidation of mechanism and discovery of new potential targets may help us have a better understanding of cisplatin resistance.

2019-08-12 | PXD013265 | Pride

Global characterization of miR-574-5p decoy to CUGBP1 in human lung cancer using a mass spectrometry proteomics approach

Project description:We aimed to characterize decoy to the RNA-binding protein CUG-RNA binding protein 1 (CUGBP1 mechanism in A549 lung cancer cells. We identified several new canonical targets of CUGBP1 but those were not regulated by miR-574-5p via the decoy mechanism. This can be explained by the localization of CUGBP1 and miR-574-5p in the nucleus, where CUGBP1 regulates alternative splicing. Next, we analyzed the 3’UTRs of potential targets and found that the decoy-dependent regulation of mPGES-1 splicing is unique. Therefore, we postulate that in A549 cells mPGES-1 is the only protein regulated by the decoy mechanism of CUGBP1 and miR-574-5p which suggests that the decoy mechanism allows the specific regulation of the expression of distinct targets.

2020-03-02 | PXD016803 | Pride

Expression profiles of X-ray responsive miRNA in human cells [mRNA data]

Project description:'MicroRNA (miRNA) is a type of non-coding RNA that regulates the expression of its target genes by interacting with the complementary sequence of the target mRNA molecules. Recent evidence has shown that genotoxic stress induces miRNA expression, but the target genes involved and role in cellular responses remain unclear. We examined the role of miRNA in the cellular response to X-ray irradiation by studying the expression profiles of radio-responsive miRNAs and their target genes in cultured human cell lines. We found that expression of miR-574-3p was induced in the lung cancer cell line A549 by X-ray irradiation. Overexpression of miR-574-3p caused delayed growth in A549 cells. A predicted target site was detected in the 3''-untranslated region of the enhancer of the rudimentary homolog (ERH) gene, and transfected cells showed an interaction between the luciferase reporter containing the target sequences and miR-574-3p. Overexpression of miR-574-3p suppressed ERH protein production and delayed cell growth. This delay was confirmed by knockdown of ERH expression. Our study suggests that miR-574-3p may contribute to the regulation of the cell cycle in response to X-ray irradiation via suppression of ERH protein production. mRNA expression were compared between the A549 cell overexpressing a radio-responsive miRNA and in the A549 cells suppressing the miRNA. Five miRNAs (miR-181d, miR-565, miR-574-3p, miR-629* and miR-766) were examined. Microarray experiments were performed with triplicate for each experiment.'

2014-03-14 | E-GEOD-30131 | biostudies-arrayexpress

Expression profiles of X-ray responsive miRNA in human cells

Project description:MicroRNA (miRNA) is a type of non-coding RNA that regulates the expression of its target genes by interacting with the complementary sequence of the target mRNA molecules. Recent evidence has shown that genotoxic stress induces miRNA expression, but the target genes involved and role in cellular responses remain unclear. We examined the role of miRNA in the cellular response to X-ray irradiation by studying the expression profiles of radio-responsive miRNAs and their target genes in cultured human cell lines. We found that expression of miR-574-3p was induced in the lung cancer cell line A549 by X-ray irradiation. Overexpression of miR-574-3p caused delayed growth in A549 cells. A predicted target site was detected in the 3'-untranslated region of the enhancer of the rudimentary homolog (ERH) gene, and transfected cells showed an interaction between the luciferase reporter containing the target sequences and miR-574-3p. Overexpression of miR-574-3p suppressed ERH protein production and delayed cell growth. This delay was confirmed by knockdown of ERH expression. Our study suggests that miR-574-3p may contribute to the regulation of the cell cycle in response to X-ray irradiation via suppression of ERH protein production. This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-03-14 | E-GEOD-30132 | biostudies-arrayexpress

Transcribed ultraconserved region 339 promotes carcinogenesis by sequestering tumor suppressor microRNAs

Project description:The transcribed ultraconserved regions (T-UCRs) are a family of long non-coding RNAs implicated in human carcinogenesis. The mechanism of action of T-UCRs and the factors regulating their expression in human cancers are poorly understood. In this study we show that high expression of uc.339 correlates with lower survival in 204 non-small cell lung cancer (NSCLC) patients. We also show that uc.339 found up-regulated in archival NSCLC samples, functions as a decoy for miR-339-3p, -663-3p and -95-5p. As a result, Cyclin E2, a direct target of these microRNAs is up-regulated, promoting cancer growth and migration. We provide evidence from cell lines and primary samples suggesting that TP53 directly regulates uc.339. Our results support a key role for uc.339 in lung cancer. 4 experimental groups in triplicate (total: 12 samples). A339= A549 infected with a lentivirus over-expressing uc.339; AE= A549 infected with an empty lentivirus (control of A339); L339= LoVo infected with a lentivirus over-expressing uc.330; LE= LoVo infected with an empty lentivirus (control of L339). 1-2-3 refer to each experiment.

2015-07-07 | E-GEOD-70540 | biostudies-arrayexpress

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