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

MiR-374a Promotes Epithelial-Mesenchymal Transition (EMT) and Metastasis of Breast Cancer

ABSTRACT: This SuperSeries is composed of the following subset Series: GSE39356: MiR-374a Promotes Epithelial-Mesenchymal Transition (EMT) and Metastasis of Breast Cancer (mRNA dataset) GSE39358: MiR-374a Promotes Epithelial-Mesenchymal Transition (EMT) and Metastasis of Breast Cancer (miRNA dataset) Refer to individual Series

ORGANISM(S): Homo sapiens

SUBMITTER: Mengfeng Li

PROVIDER: E-GEOD-39359 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

MiR-374a Promotes Epithelial-Mesenchymal Transition (EMT) and Metastasis of Breast Cancer (miRNA dataset)

Project description:This experiment is designed to screen miRNAs that are deregulated during breast cancer metastasis. Comparatively analyzing miRNAs in parental MDA-MB-435 cells and cells obtained from its lung metastases, 23 miRNAs expressed differentially, among which 12 were elevated and 11 were down-regulated. Total RNA were extracted from parental MDA-MB-435 cells and cells obtained from its lung metastases after 30 days inoculation. Two biological replications for each treatment.

2012-07-13 | E-GEOD-39358 | biostudies-arrayexpress

MiR-374a Promotes Epithelial-Mesenchymal Transition (EMT) and Metastasis of Breast Cancer (mRNA dataset)

Project description:This experiment is designed to evaluate gene expression alterations following miR-374a transduction in breast cancer cells. We find a significant elevation of Wnt/β-catenin signaling transcriptional targets. Total RNA were extracted from MCF-7 breast cancer cells stably transduced with miR-374a precursor or vector control. Two biological replications for each treatment.

2012-07-13 | E-GEOD-39356 | biostudies-arrayexpress

AEG-1 silencing induced gene expression alteration in glioma cells

Project description:This experiment is designed to evaluate gene expression alteration following AEG-1 (MTDH) silencing in glioma cells. AEG-1 is found to be a potential regulator through interaction with other transcription factor. We intended to investigate the enriched transcription factor dependent downstream gene sets regulated by AEG-1 form the differential expressed genes we obtained from AEG-1 silencing. Total RNA were extracted from U87MG glioma cells stably silencing AEG-1 and correspondent pSuper Retro vector cells respectively. Passage 5 of the indicated cells after infection and selection were harvested for RNA extraction.

2011-07-12 | E-GEOD-29952 | biostudies-arrayexpress

Antagonizing miR-128 abrogates chemoresistance-associated metastasis and is therapeutic in non-small cell lung cancer [mRNA]

Project description:This experiment is designed to evaluate gene expression alteration and significant pathway(s) following miR-128 transduction in A549 lung cancer cells. We find several significant pathways, including the Wnt/β-catenin signaling and TGF-β signaling activated by miR-128 overexpression. Total RNA were extracted from A549 lung cancer cells stably transduced with miR-128 precursor or vector control and subjected to mRNA microarray (Agilent-014850 Whole Human Genome Microarray 4x44K) analysis, with two biological replications for each treatment.

2015-04-10 | E-GEOD-67728 | biostudies-arrayexpress

Antagonizing miR-128 abrogates chemoresistance-associated metastasis and is therapeutic in non-small cell lung cancer [miRNA]

Project description:This experiment is designed to screen miRNAs that are deregulated during chemoresistance-associated metastasis of lung cancer cells. Chemoresistant metastatic in vivo tumor model of A549-luc-Vector cells was established after four rounds of cisplatin (CDDP) treatments compared to corresponding control solvent treatments. Upon examining profiles of miRNA expression differential between tumor-derived cultured cells from the Ctrl-4th and CDDP-4th treatments, most markedly upregulated and downregulated miRNAs in chemoresistant, metastatic A549-luc-CDDP-4th cells were identified. In order to establish a chemoresistant in vivo tumor model, after inoculation of A549-luc-Vector cells, cisplatin (CDDP) or control solvent was intraperitoneally (i.p.) injected six rounds in a two-week period and cells were isolated from corresponding resultant tumors, cultured and re-transplanted into syngeneic mice to receive the next round of treatment. In our experimental model, human lung cancer xenografts developed chemoresistance in the third round of CDDP treatment (CDDP-3rd) and chemoresistance-associated metastases following the fourth round of treatment. Tumor-derived cultured cells from Ctrl-4th and CDDP (cisplatin)-4th treatment were subjected to miRNA array (Agilent-031181 human miRNA (8*60k) V16.0) analysis, with two biological replications for each treatment.

2015-04-10 | E-GEOD-67727 | biostudies-arrayexpress

miR-1245 induce genomic instability

Project description:This experiment is design to evaluate genomic alteration following stably expression of miR-1245, stably knock down of BRCA2 is setup as a positive control Primary normal breast epithelial cells (NBEC) were collected from the mammoplasty material of a 30-year-old woman at the Department of Plastic Surgery, the First Affiliated Hospital of Sun Yat-sen University (P. R. China), in accordance with rules and regulations concerning ethical issues on research use of human subjects in China, and were cultured in the Keratinocyte serum-free medium (Invitrogen, Carlsbad, CA) supplemented with epithelial growth factor, bovine pituitary extract and antibiotics (120 µg/mL streptomycin and 120 µg/mL penicillin). NBEC were infected with virus produced from retro vector pMSCV-miR1245 or empty pMSCV vector; or pSuper Retro BRCA2 shRNA, or pSuper Retro empty vector. After 2 days infection and 3 days culture, genomic DNA was isolated using the QIAamp DNA Mini Kit (QIAGENE, Valencia, CA). CGH microarray hybridization, data generation and normalization were performed in Shanghai Biochip Corporation.

2011-03-23 | E-GEOD-26715 | biostudies-arrayexpress

Antagonizing miR-128 abrogates chemoresistance-associated metastasis and is therapeutic in non-small cell lung cancer

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-04-10 | E-GEOD-67729 | biostudies-arrayexpress

miR-182 induced gene expression alteration in glioma cells

Project description:This experiment is designed to evaluate gene expression alteration following miR-182 transfection in glioma cells. We find a significant elevation of NF kappa B transcriptional targets. Total RNA were extracted from SNB-19 glioma cells transfected with miR-182 mimic oligo or miRNA mimic negative control 36 hours after transfection, two biological replications for each treatment.

2011-11-15 | E-GEOD-33293 | biostudies-arrayexpress

SMAD2/3 mediated transcripts in A549 cells

Project description:This experiment is designed to evaluate gene expression alteration following silencing SMAD2/3 and overexpressing CCT6A in A549 lung cancer cells. Total RNA were extraced from indicated stable cell lines treated with or with out TGF-Î²

2016-08-10 | E-GEOD-61132 | biostudies-arrayexpress

Expression analysis of Streptomyces avermitilis NRRL8165 delta-aveI mutant

Project description:Investigation of whole genome gene expression level changes in Streptomyces avermitilis delta-aveI mutant, compared to the wild-type strain. The mutants analyzed in this study are further described in Chen L, Lu Y., Chen J, Zhang W, Shu D, Qin Z, Yang S, Jiang W. (2008) Characterization of a negative regulator AveI for avermectin biosynthesis in Streptomyces avermitilis NRRL8165. Appl Microbiol Biotechnol 80(2): 277-86. A six chip study using total RNA recovered from three separate Streptomyces avermitilis NRRL8165 and three separate cultures of a Streptomyces avermitilis NRRL8165 delta-aveI (delta-l) mutant. 3 separate RMA normalizations performed, one for each pair of control and mutant samples.

2010-05-16 | E-GEOD-16892 | biostudies-arrayexpress

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