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

PKCÎ´ regulates the transformed growth of K-ras dependent lung cancer cells through regulation of integrin Î±VÎ²3 expression

ABSTRACT: To explore how PKCÎ´ regulates tumorigenesis, we performed mRNA expression analysis of four KRAS mutant NSCLC cell lines that stably express scrambled shRNA or PKCÎ´ targeted shRNA Four human lung cancer cell lines (A549, H441, H460 and H2009) with scrambled and PKC-delta knock down (shRNA), in triplicate.

ORGANISM(S): Homo sapiens

SUBMITTER: Aik Choon Tan

PROVIDER: E-GEOD-72788 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

PKCδ regulates the transformed growth of K-ras dependent lung cancer cells through regulation of integrin αVβ3 expression

Project description:To explore how PKCδ regulates tumorigenesis, we performed mRNA expression analysis of four KRAS mutant NSCLC cell lines that stably express scrambled shRNA or PKCδ targeted shRNA

2016-09-01 | GSE72788 | GEO

Identification of FOSL1 transcriptional targets in mutant KRAS lung adenocarcinoma cells

Project description:Mutant KRAS lung adenocarcinoma cells, H2009, were depleted of FOSL1 by a specific shRNA and its transcriptome was profiled

2017-06-12 | GSE76290 | GEO

PHF19 shRNA or scrambled control shRNA

Project description:PHF19 shRNA or scrambled control shRNA

| PRJNA1070967 | ENA

MicroRNA expression analysis of integrin-linked kinase gene silencing in A2780 cell line

Project description:Available evidence has suggested that integrin-linked kinase (ILK) underwent over-expression in ovarian cancer while specific gene silencing of ILK resulted in apoptosis of ovarian cancer cells. Here, potential mechanisms in which ILK induces cell apoptosis was explored from the perspective of microRNA (miRNA) expression. Alteration in global miRNA expression profile was detected by miRNA microarray technique after ILK shRNA expression lentivirus was transfected into A2780 cells (n = 3). Additionally, the A2780 cells infected by scrambled shRNA lentivirus were treated as negtive control (n = 3).

2016-06-28 | E-GEOD-83721 | biostudies-arrayexpress

Endoxifen Downregulates AKT Phosphorylation Through Protein Kinase C Beta 1 in ER+/HER2- Breast Cancer

Project description:In phase I/II clinical trials, Z-endoxifen demonstrated substantial oral bioavailability and promising antitumor activity in endocrine-refractory estrogen-receptor positive breast cancer (ER+ BC) and other solid tumors, with plasma concentrations reportedly as high as 5 ï�M. Therefore, we explored the potential mechanisms of Z-endoxifen antitumor activity that extends beyond ERÎ± inhibition. In estrogen unstimulated aromatase-expressing ER+/human epidermal growth factor 2 receptor negative (HER2-) MCF7AC1 BC cells, Z-endoxifen at 5 ï�M, but not ERï�¡-targeting 0.01 and 0.1 ï�M concentrations inhibited growth and induced apoptosis, suggesting an ERÎ±-independent effect. Utilizing an unbiased mass spectrometry approach, we explored Z-endoxifen effects on other signaling pathways. Z-endoxifen at 5 ÂµM profoundly altered the phosphoproteome with minimal impact on total proteome. Computational analysis revealed Protein kinase C beta (PKCï�¢) and AKT1 as the prevalent upstream kinases for Z-endoxifen-downregulated protein phosphorylations. Notably, in ER+/HER2- BC models, Z-endoxifen at 5 ï�M attenuated AKTSer473 and AKT substrates in vitro in the presence of insulin and PKC agonist PMA and in vivo. Further, Z-endoxifen inhibited PKCï�¢1 kinase activity compared to other PKC isoforms in vitro and bound to PKCÎ²1. While PMA stimulated PKCï�¢1Ser661 phosphorylation correlated with AKTSer473 and AKT substrate phosphorylation, Z-endoxifen at 5 ï�M uniquely blocked these effects and induced PKCÎ²1 protein degradation. siRNA-mediated PKCï�¢1 knockdown attenuated AKTSer473 phosphorylation, suggesting PKCÎ²1-mediated suppression of AKT signaling by Z-endoxifen. Further, Z-endoxifen at 5 ï�M replicates the pan-AKT inhibitor MK-2206 effects on apoptosis. These findings implicate PKCÎ²1 as a novel Z-endoxifen substrate responsible for suppressing AKT signaling and inducing apoptosis in breast cancer.

2024-01-26 | PXD035007 | Pride

Identification of Zdhhc20 knock-down cell palmitome

Project description:An shRNA screen to search for the mediators of pancreatic cancer metastasis identified palmitoyl transferase ZDHHC20 as a protein that mediates this process by promoting the outgrowth of metastatic cells in vivo. We sought to identify the changes in the palmitome of the cells expessing scrambled shRNA or shRNAs targeting Zdhhc20.

2023-02-09 | PXD038048 | Pride

PRMT5 inhibition increases PD-L1 expression and immunoresistance in lung cancer

Project description:Purpose: We sequenced mRNA from 3 biological replicates each of NCI-H460 lung adenocarcinoma cell lines expressing shRNA against GFP (control) or PRMT5.We then determined differential gene expression to identify the relationship between PRMT5 expression and tumorigenesis. Methods: PRMT5 shRNA and control shRNA NCI-H460 cells were generated by lentivirus targeting PRMT5 or GFP(control), in triplicate,using illumina Novaseq™ 6000. Results:PRMT5 specific knockdown cells were enriched in the negative regulation of T cells and type I IFN response,we found that negative regulation of T cell molecules like Arg2, CD274 and IDO1 were increased in the PRMT5 shRNA group compared with the control group.

2022-02-08 | GSE178521 | GEO

Affymetrix U133Plus2.0 data sets of Human Myeloma Cellline JJN3 with non-specific, scrambled shRNA or CKS1B shRNA

Project description:This series represents Affymetrix U133Plus2.0 data sets of JJN3 transduced with levivirus expressing non-specific scrambled shRNA or CKS1B shRNA Keywords: JJN3 CKS1B shRNA

2006-03-31 | GSE3369 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of ADORA1 knockdown and scrambled-shRNA control cells' Transcriptomes

Project description:Expression profiles of ADORA1-shRNA-transfected Sk-mel-28 human melanoma cell line and scrambled-shRNA control cells

2020-07-23 | GSE134493 | GEO

Identification of chromatin accessibility domains in EMT and breast cancer stem cell formation.

Project description:Epithelial-mesenchymal transition (EMT), the process whereby cells gain migratory and invasive properties characteristic of mesenchymal cells, plays a central role in embryogenesis and wound healing in a wide range of tissues. However, EMT has also been linked to the formation of cancer stem cells (CSCs). Many of the signaling pathways involved in EMT have also been implicated in CSC formation but the processes that contribute uniquely to CSC formation remain elusive. We have previously demonstrated that PKCÎ¸ activation is critical for EMT induction and concomitant CSC formation in the breast cancer luminal epithelial cell line, MCF7. To discover how PKC-induced alterations in the epigenome influence the EMT and CSC formation in MCF-7 cells, we employed a combination of expression profiling and Formaldehyde Assisted Regulatory Elements (FAIRE)-sequencing in order to reveal novel links between gene expression and DNA accessibility changes after PKCÎ¸ activation. We found that, during EMT, increases in accessibility generally occurred in regions away from transcription start sites, low in CpG, enriched with chromatin marks of enhancer elements and motifs for FOX, AP1, TEAD and AP2. Increases in FOX and AP-1 motif accessibility were associated with genes that exhibited increased expression in CSC, while increased AP-2 accessibility was associated with genes that had higher expression in non-CSCs. This study revealed novel regions of DNA accessibility induced by PKC that contribute to the understanding of how epigenomic plasticity of cells undergoing EMT leads to the activation of genes that drive the CSC program. 2 biological samples were analysed with 2 biological replicates each and a mixed total input.

2016-03-10 | E-GEOD-71023 | 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