Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA sequencing of BRCA2 and/or RB1 knockout LNCaP cells

ABSTRACT: Human prostate cancer LNCaP cells infected with Lentivirus carried huamn BRCA2 gRNA alone or in combination with lentivirus carrying human RB1 shRNA. Infected cell were selcted by drug selection and the knockdown were confirm by westernblot or qPCR

ORGANISM(S): Homo sapiens

PROVIDER: GSE114153 | GEO | 2020/05/07

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

RNA sequencing of BRCA2 and/or RB1 knockout LNCaP cells

Project description:RNA sequencing of BRCA2 and/or RB1 knockout LNCaP cells

| PRJNA470609 | ENA

Mechanism of TP53 and RB1 inactivation-induced neuroendocrine phenotype transformation in TKI-resistant lung adenocarcinoma

Project description:In order to study the mechanism of co-inactivation of RB1 and TP53 in the transformation of lung adenocarcinoma to small cell lung cancer, we established the NCI-H1975 cell line with RB1 knockdown.NCI-H1975 cells were cultured and infected with lentivirus expressing RB1-shRNA (n=3) or pLKO.1-shRNA (n=3), We then performed transcriptome sequencing (RNA-seq) on the above cells.

2023-08-20 | PXD042073 | Pride

RNA sequencing of RRM2 overexpressing in LNCaP cells

Project description:Human prostate cancer LNCaP cells stably overexpress RRM2. Overexpression of RRM2 were confirm by westernblot or qPCR. Transfected cells were prepared for RNA-seq.

2020-02-20 | GSE117922 | GEO

Mechanism of TP53 and RB1 inactivation-induced neuroendocrine phenotype transformation in TKI-resistant lung adenocarcinoma

2023-07-25 | GSE232387 | GEO

Combined loss of BRCA2 and RB1 leads to aggressive prostate cancer mediated by WNK1

Project description:Combined loss of BRCA2 and RB1 leads to aggressive prostate cancer mediated by WNK1

| PRJNA464438 | ENA

Effects of BRCA2 cis-regulation in normal breast and cancer risk amongst BRCA2 mutation carriers

Project description:This SuperSeries is composed of the following subset Series: GSE32124: Effects of BRCA2 cis-regulation in normal breast and cancer risk amongst BRCA2 mutation carriers [expression data] GSE32258: Effects of BRCA2 cis-regulation in normal breast and cancer risk amongst BRCA2 mutation carriers [SNP data] Refer to individual Series

2012-02-01 | E-GEOD-32259 | biostudies-arrayexpress

Analysis of gene expression (RNAseq) from shTP53:RB1 LNCaP/AR cell lines

Project description:Some cancers evade targeted therapies through a mechanism known as lineage plasticity, whereby tumor cells acquire phenotypic characteristics of a cell lineage whose survival no longer depends on the drug target. Here we show, using in vitro and in vivo prostate cancer models, that these tumors can develop resistance to the antiandrogen drug enzalutamide by a phenotypic shift from androgen receptor (AR) dependent luminal epithelial cells to AR independent basal-like cells. This lineage plasticity is enabled by loss of TP53 and RB1 function, is mediated by increased expression of the reprogramming transcription factor SOX2 and can be reversed by restoring TP53 and RB1 function or by inhibiting SOX2 expression. Thus, mutations in tumor suppressor genes can create a state of increased cellular plasticity that, when challenged with antiandrogen therapy, promotes resistance through lineage switching.

2017-01-06 | GSE89226 | GEO

BRCA2 ChIP-seq hTert-HME1 cell line

Project description:Individuals with a single functional copy of the BRCA2 tumor suppressor have elevated risks for breast, ovarian, and other solid tumor malignancies. The exact mechanisms of carcinogenesis due to BRCA2 haploinsufficiency remain unclear, but one possibility is that at-risk cells are subject to acute periods of decreased BRCA2 availability and function ("BRCA2-crisis"), which may contribute to disease. Here, we establish an in vitro model for BRCA2-crisis that demonstrates chromatin remodeling and activation of an NF-κB survival pathway in response to transient BRCA2 depletion. Mechanistically, we identify BRCA2 chromatin binding, histone acetylation, and associated transcriptional activity as critical determinants of the epigenetic response to BRCA2-crisis. These chromatin alterations are reflected in transcriptional profiles of pre-malignant tissues from BRCA2 carriers and, therefore, may reflect natural steps in human disease. By modeling BRCA2-crisis in vitro, we have derived insights into pre-neoplastic molecular alterations that may enhance the development of preventative therapies.

2019-08-07 | GSE133450 | GEO

HOTAIR or shHOTAIR lentiviral infected prostate cancer cells [ChIP-Seq]

Project description:LNCaP prostate cancer cells were infected by lentivirus expressing either ctrl or HOTAIR, and the cells were cultured in hormone-deprived condition (Ethl) or in the presence of androgen (R1881). C4-2B prostate cancer cells were infected by lentivirus expressing either shCtrl or shHOTAIR, and the cells were cultured in hormone-deprived condition (Ethl) or in the presence of androgen (R1881).

2015-10-01 | GSE61268 | GEO

HOTAIR lentiviral infected prostate cancer cells

Project description:LNCaP prostate cancer cells were infected by lentivirus expressing either ctrl or HOTAIR. The cells were cultured either in hormone-deprived condition (Ethl) or in the presence of androgen( R1881).

2015-10-01 | GSE61269 | GEO

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