Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profiles in KRAS mutant A549 cells after BI-2536 and fasudil combination treatment

ABSTRACT: To identify the potential mechanisms of enhanced activity of combined inhibition of PLK1 and ROCK, we conducted a microarray analysis on gene expression profiles in KRAS mutant A549 cells. We used Affymetrix GeneChip PrimeView Human Gene Expression array to detail gene expression after indicated treatments and identified the molecular mechanism during this process to facilitate further studies.

ORGANISM(S): Homo sapiens

PROVIDER: GSE60887 | GEO | 2014/08/29

SECONDARY ACCESSION(S): PRJNA259746

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

gene expression profiles in KRAS mutant A549 cells after BI-2536 and fasudil combination treatment

Project description:To identify the potential mechanisms of enhanced activity of combined inhibition of PLK1 and ROCK, we conducted a microarray analysis on gene expression profiles in KRAS mutant A549 cells. We used Affymetrix GeneChip PrimeView Human Gene Expression array to detail gene expression after indicated treatments and identified the molecular mechanism during this process to facilitate further studies. A549 cells were treated with vehicle control, BI-2536 (4 nM), fasudil (20 ÂµM), or the combination of BI-2536 and fasudil for 6 h. Samples were obtained from three independent biological replicates.RNA from each sample was labeled and hybridized using Affymetrix GeneChip PrimeView Human Gene Expression array.

2014-08-29 | E-GEOD-60887 | biostudies-arrayexpress

A proteomic and phosphoproteomic landscape of KRAS mutant cancers identifies combination therapies

Project description:KRAS mutant cancers, which feature the activation of multiple phosphorylation signaling pathways, remain a major challenge for cancer therapy. This study provides a landscape of the proteomics and phosphoproteomics of KRAS mutant cancers by analyzing different KRAS mutant human cancer cell lines across different tissues types. By integrating multi-omics analysis, we identify different robust subsets, which recapitulate the histological, pathological and prognostic features of human cancers.

2021-06-23 | PXD026892 | iProX

BI-3406, a potent and selective SOS1::KRAS interaction inhibitor, is effective in KRAS-driven cancers through combined MEK inhibition

Project description:KRAS is the most frequently mutated driver of pancreatic, colorectal, and non-small cell lung cancers. Direct KRAS blockade has proven challenging and inhibition of a key downstream effector pathway, the RAF-MEK-ERK cascade, has shown limited success due to activation of feedback networks that keep the pathway in check. We hypothesized that inhibiting SOS1, a KRAS activator and important feedback node, represents an effective approach to treat KRAS-driven cancers. We report the discovery of a highly potent, selective and orally bioavailable small-molecule SOS1 inhibitor, BI-3406, that binds to the catalytic domain of SOS1 thereby preventing the interaction with KRAS. BI-3406 reduces formation of GTP-loaded RAS and limits cellular proliferation of a broad range of KRAS-driven cancers. Importantly, BI-3406 attenuates feedback reactivation induced by MEK inhibitors and thereby enhances sensitivity of KRAS-dependent cancers to MEK inhibition. Combined SOS1 and MEK inhibition represents a novel and effective therapeutic concept to address KRAS-driven tumors.

2020-08-20 | GSE128385 | GEO

Determining the KRAS-regulated kinome in PDAC

Project description:Oncogenic KRAS drives cancer growth by activating diverse signaling networks, not all of which have been fully delineated. We set out to establish a system-wide profile of the KRAS-regulated kinase signaling network (kinome) in KRAS-mutant pancreatic ductal adenocarcinoma (PDAC). We knocked down KRAS expression in a panel of six cell lines, and then applied Multiplexed Inhibitor Bead/Mass Spectrometry (MIB/MS) chemical proteomics to monitor changes in kinase activity and/or expression. We hypothesized that depletion of KRAS would result in downregulation of kinases required for KRAS-mediated transforming activities, and in upregulation of other kinases that could potentially compensate for the deleterious consequences of the loss of KRAS. We identified 15 upregulated and 13 downregulated kinases in common across the panel. In agreement with our hypothesis, all 15 of the upregulated kinases have established roles as cancer drivers (e.g., SRC, TGFBR1, ILK), and pharmacologic inhibition of the upregulated kinase, DDR1, suppressed PDAC growth. Interestingly, 11 of the 13 downregulated kinases have established driver roles in cell cycle progression, particularly in mitosis (e.g., WEE1, Aurora A, PLK1). Consistent with a crucial role for the downregulated kinases in promoting KRAS-driven proliferation, we found that pharmacologic inhibition of WEE1 also suppressed PDAC growth. The unexpected paradoxical activation of ERK upon WEE1 inhibition led us to inhibit both WEE1 and ERK concurrently, which caused further potent growth suppression and enhanced apoptotic death than WEE1 inhibition alone. We conclude that system-wide delineation of the KRAS-regulated kinome can identify potential therapeutic targets for KRAS-mutant pancreatic cancer.

2022-02-17 | PXD025819 | Pride

Genome-wide maps of histone H3K27 acetylation in A549 and MSR-A549 cells.

2019-03-28 | GSE96780 | GEO

mRNA expression profile of A549 cells and MSR-A549 cells with or without JQ1 treatment

Project description:To establish effective multitargeted KRAS pathway therapy, we analyzed mediators of acquired resistance to chronic momelotinib and MEK inhibitor exposure in A549 cells. Since inhibitor resistance was completely reversible after drug withdrawal for several passages, suggesting epigenetic reprogramming, we investigated whole mRNA expression profiles in A549, momelotinib and selumetinib resistant (MSR)-A549 cells and MSR-A549 cells following drug withdrawal for 10 days. In parallel, we also examined mRNA expression profiles of MSR-A549 cells treated with the BET inhibitor JQ1, to identify specific targets regulated by H3K27 acetylation.

2019-03-28 | GSE96779 | GEO

UHRF1 is a mediator of KRAS driven oncogenesis in lung adenocarcinoma [CRISPR_screen]

Project description:We performed a focused CRISPR in KRAS mutant lung cancer cells (A549) using a minipool sgRNA library targeting 80 lung cancer specific tumor suppressor genes and 12 control genes. This screen identified tumor suppressor genes regulated by Uhrf1 in KRAS mutant lung cancer.

2023-05-25 | GSE233401 | GEO

Targeting KRAS mutant cancers with a covalent G12C-specific inhibitor

Project description:We report RNAseq gene expression data following ARS-1620 treatment and shKRAS expressing cells (NCI-H358). We also compare gene expression changes following treatment with ARS-1620 or trametinib in NCI-H358, LU65 (KRAS-G12C+), and A549 (KRAS-G12S+) cells. Additionally we report a time course (4, 24, 48hr) of ARS-1620 and trametinib treated NCI-H358 cells.

2018-01-24 | GSE103021 | GEO

The phospholipid transporter PITPNC1 links KRAS to MYC to prevent autophagy in lung and pancreatic cancer

Project description:RNA profiling of mut KRAS lung cancer cells (A549) where PITPNC1 is depleted using two specific shRNAs

2023-08-10 | GSE205767 | GEO

Transcriptomic analysis of SiHa cells stably expressing shCtrl or shSYT7

Project description:GeneChip PrimeView Human PathArrayTM was performed using the SiHa cells-stably expressing shCtrl or shSYT7. To investigate the underlying mechanism of tumor-suppressive phenotypes of CESC with SYT7 knockdown, we used GeneChip PrimeView Gene Expression Array that could detect expression profiling of over 36,000 transcripts and variants using the SiHa-shCtrl and shSYT7-cDNAs

2022-04-11 | GSE200526 | 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