Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MCF7 cells: empty vector (Neo) vs. PAR4 overexpression vector transfected before and after 100nM docetaxel treatment

ABSTRACT: The aim of this study was evaluate the transcriptome changes in the comparison between MCF7 cells with increased expression of PAR-4 and the control cells before and after docetaxel treatment . The results generated could be of particular interest for the understanding the action of PAR-4 in chemosensitivity, especially to increase the specificity and effectiveness of drug treatment and overcoming resistance to chemotherapy.

ORGANISM(S): Homo sapiens

PROVIDER: GSE81064 | GEO | 2017/05/04

SECONDARY ACCESSION(S): PRJNA320407

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Silenced LINC01963 enhanced the chemosensitivity of prostate cancer cells to docetaxel by sponging miR-216b-5p to inhibit TrkB protein level

Project description:Long noncoding RNAs (lncRNAs) affect docetaxel chemosensitivity. However, the biological role and regulatory mechanisms of lncRNAs in docetaxel-resistant prostate cancer remain unclear. Differences in lncRNAs were evaluated by lncRNA sequencing and evaluated using quantitative real-time polymerase chain reaction, and TrkB expression was measured through Western blot analysis. Proliferation was measured using the MTS, while apoptosis and cell cycle were measured using flow cytometry. Additionally, migration and invasion were measured using transwell assays. Forty-eight female BALB/c nude mice were used for subcutaneous tumorigenicity and lung metastasis assays. We found that LINC01963 was overexpressed in the PC3-DR cells. LINC01963 silencing enhanced the chemosensitivity of PC3-DR to docetaxel and inhibited tumorigenicity and lung metastasis, while LINC01963 overexpression enhanced the chemoresistance of PC3 cells to docetaxel. It was found that LINC01963 sponges miR-216b-5p. The miR-216b-5p inhibitor reversed the suppressive effect of sh-LINC01963 on PC3-DR cell proliferation, migration, and invasion. Furthermore, miR-216b-5p can bind to the 3’-UTR of NTRK2 and inhibit TrkB protein levels. TrkB enhances docetaxel resistance in prostate cancer and reverses the effects of LINC01963 silencing and miR-216b-5p overexpression. In conclusion, silencing LINC01963 enhanced the chemosensitivity of PC3-DR to docetaxel by sponging miR-216b-5p to inhibit TrkB protein levels.

2021-12-13 | GSE190648 | GEO

Transcription Factor Network Reveals New Treatments for Prostate Cancer Docetaxel Drug Resistance

Project description:Overcoming drug resistance is critical increasing the survival rate for prostate cancer (PCa). In this study, we modeled docetaxel resistance using two PCa cell lines, DU145 and PC3. We conducted both single cell and bulk RNA sequencing. We constructed a transcription factor (TF) network for the docetaxel sensitive and resistant variants for all cell lines and sequencing methods resulting in 8 networks. We identified shared edges and nodes that represent a shared TF network for PCa that modeled the changes after acquiring drug resistance. Using this shared TF network, we identified drivers of the resistant phenotype. Interestingly, the network constructed from the bulk sequencing dataset revealed different TF drivers of resistance compared with the network constructed from the single cells. We validated the results constructed from the single cells to demonstrate the validity of the single cell sequenced TF network. We targeted GABPA (only identified in the single cell constructed network) and successfully re-sensitized both cell lines to docetaxel treatment. Additionally, we conducted connectivity map analysis to identify potential drugs that disrupt the resistant networks. We identified trichostatin A as a potential combination treatment using the single cell sequenced network. Combination treatment of trichostatin A and docetaxel, both in vitro and in vivo PCa models decreased tumor growth. These results suggest by analyzing a population of resistant cells, identification of drivers and novel treatments is possible.

2023-04-01 | GSE149681 | GEO

Expression data from prostate cancer cell lines C4-2B (docetaxel sensitive) and TaxR (docetaxel resistant) cells

2013-08-01 | GSE47040 | GEO

Expression data from prostate cancer cell lines C4-2B (docetaxel sensitive) and TaxR (docetaxel resistant) cells

Project description:Prostate cancer C4-2B cells were cultured in docetaxel in a dose-escalation manner. After nine months selection, cells were able to divide freely in 5 nM docetaxel, with a specific sets of genes been deregulated. We performed global gene expression analysis by cDNA microarrays to identify genes responsible for docetaxel resistance in TaxR cells. Docetaxel resistant TaxR cells were selected from C4-2B cells during long time docetaxel treatment. Genes responsible for docetaxel resistance were identified using C4-2B vs. TaxR RNA extraction and hybridization on Affymetrix microarrays.

2013-08-01 | E-GEOD-47040 | biostudies-arrayexpress

Identificatinon of differentially expressed genes in Docetaxel-resistant cell lines PC3 and DU145 after combination treatment with RU486 and docetaxel

Project description:Upregulation of the glucocorticoid receptor (GR) has been identified as a possible bypass mechanism in CRPC. Recently, it has been demonstrated that the combination of docetaxel with mifepristone (D+M), an inhibitor of the GR, reinduces sensitivity to docetaxel in docetaxel resistant cell models. This study was designed to uncover and characterize molecular mechanisms responsible for this observation.

2023-12-31 | GSE233647 | GEO

Expression data from prostate cancer Docetaxel-resistant cells

2012-10-02 | GSE36135 | GEO

Expression data from docetaxel-resistant prostate cancer cell lines

Project description:Docetaxel-based chemotherapy is the standard first-line therapy in metastatic castration-resistant prostate cancer. However, most patients eventually develop resistance to this treatment. The aim of the study was to identify key molecular genes and networks associated with docetaxel resistance in 2 models of docetaxel-resistant castration-resistant prostate cancer cell lines.

2012-01-01 | GSE33455 | GEO

Expression data from Docetaxel-resistant prostate cancer cells

Project description:Docetaxel is the standard first line therapy for hormone-refractory prostate cancer patients. Here we generated models of Docetaxel resistance in prostate cancer cells to study the molecular pathways that drive the acquisition of resistance to this therapy. We used microarrays to detail the global program of gene expression underlying the acquisition of Docetaxel resistance in prostate cancer cells. Parental Docetaxel-sensitive prostate cancer cell lines (DU145 and 22Rv1) and selected Docetaxel-resistant cells (DU145-DR and 22Rv1-DR) were harvested for RNA extraction and hybridization on Affymetrix microarrays. Samples were analyzed in triplicates in order to increase the resolution of expression profiles.

2012-10-02 | E-GEOD-36135 | biostudies-arrayexpress

Docetaxel inhibits epithelial-mesenchymal transition in human mammary cells

Project description:Epithelial–mesenchymal transition (EMT) is a reversible and dynamic biological process in which epithelial cells acquire mesenchymal characteristics including enhanced stemness and migratory ability. EMT can facilitate cancer metastasis and is a known driver of cellular resistance to common chemotherapeutic drugs such as docetaxel. Current chemotherapeutic practices such as docetaxel treatment can promote EMT and increase the chance of tumour recurrence and resistance, calling for new approaches in cancer treatment. Here we show that prolonged docetaxel treatment at a sub-IC50 concentration inhibits EMT in immortalized human mammary epithelial (HMLE) cells. Using immunofluorescence, flow cytometry, and bulk transcriptomic sequencing to assess EMT progression, we analysed a range of cellular markers of EMT in docetaxel-treated cells and observed an upregulation of epithelial markers and downregulation of mesenchymal markers in the presence of docetaxel. This finding suggests that docetaxel may have clinical applications not only as a cytotoxic drug but also as an inhibitor of EMT-driven metastasis and multidrug resistance, depending on the concentration of its use.

2023-11-05 | GSE247028 | GEO

docetaxel response predic Illumina

Project description:Using gene expression profiling of mammary tumors generated in a mouse model for BRCA1-associated breast cancer we have searched for markers that correlate with response to the anti-cancer drugs docetaxel or cisplatin. To validate the results, the analysis was done on 2 different platforms (39K Mouse Exonic Evidence Based Oligonucleotide (MEEBO), and 45K Illumina Sentrix mouse V6 single-channel bead arrays). Moreover, we analyzed mouse mammary tumors that had acquired docetaxel resistance on the MEEBO platform.

2011-10-26 | E-MTAB-413 | 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