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

HCT116 colon cancer CRC in high and low glucose

ABSTRACT: HCT116 Kras WT and Kras G13D isogenic pair cell lines were cultured in either 25 mM or 1 mM for one week. Two independent replicate samples for each cell line and for each treatment were profiled using Affymetrix HG U133 plus 2.0 arrays

ORGANISM(S): Homo sapiens

SUBMITTER: E.Alejandro Sweet-Cordero

PROVIDER: E-GEOD-31084 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

HCT116 colon cancer CRC in high and low glucose

Project description:HCT116 Kras WT and Kras G13D isogenic pair cell lines were cultured in either 25 mM or 1 mM for one week.

2012-07-01 | GSE31084 | GEO

Rescue of KRAS suppression in HCT116 colon cancer cell line

Project description:Cancer cells that express oncogenic alleles of RAS typically require sustained expression of the mutant allele for survival, but the molecular basis of this oncogene dependency remains incompletely understood. To identify genes that can functionally substitute for oncogenic RAS, we systematically expressed 15,294 open reading frames in a human KRAS-dependent colon cancer cell line engineered to express an inducible KRAS-specific shRNA. We found 147 genes that promoted survival in the setting of KRAS suppression. In this model, the transcriptional co-activator YAP1 rescued cell viability in KRAS-dependent cells upon suppression of KRAS and was required for KRAS-induced cell transformation. Acquired resistance to Kras suppression in a Kras-driven murine lung cancer model also involved increased YAP1 signaling. KRAS and YAP1 converge on the transcription factor FOS and activate a transcriptional program involved in regulating the epithelial-mesenchymal transition (EMT). Together, these findings implicate transcriptional regulation of EMT by YAP1 as a significant component of oncogenic RAS signaling. We used microarrays to compare gene expression in HCT116 cells in which we suppressed KRAS expression doxycycline-inducible shRNA targeting KRAS compared to cells treated with media alone (no shKRAS induced). We express KRAS, LacZ, and YAP1 in each condition to identify genes transcriptionally involved in the rescue of KRAS suppression. HCT116 cells harboring doxycycline-inducible shKRAS (HCTtetK) expressing either LacZ, KRAS, or YAP1, were treated with doxycycline for 30 hours to suppress KRAS. Untreated (no doxycycline) cells expressing each ORF were used as control. Total RNA was collected using PerfectPure RNA Cultured Cell Kit (5Prime) and expression profiling was performed on Human Genome U133A 2.0 Array (Affymetrix) using the Dana Farber Cancer Institute Microarray Core.

2014-07-22 | E-GEOD-55942 | biostudies-arrayexpress

Gene expression profile of HCT116 exposed to chronic hypoxia

Project description:To identify genes involved in survival to prolonged hypoxia we exposed HCT116 to hypoxia for 3 days. Control cells were exposed to normoxic conditions. HCT116 colon cancer cells were serum starved and exposed to hypoxia (1%O2) or normoxia (21%O2) for 3 days.

2013-01-18 | E-GEOD-43608 | biostudies-arrayexpress

Kras mutant v WT with or without AZD6244 in vivo study

Project description:HCT116 (kRas mt) cells and HKH2 (Kras wt) cells were implanted into the right and left flanks of nude mice and either untreated or treated with a MEK inhibitor (AZD6244) over time. Tumours were excised and harvested for RNA extraction at the end of the experiment and hybridised to the Colorectal DSA.

2012-04-30 | E-MEXP-3557 | biostudies-arrayexpress

Induction of ER stress in HCT116 colon cancer cells

Project description:To investigate the role of p53 and DICER in the induction of ER stress, wildtype, p53 knockout or DICER mutant HCT116 colon cancer cells were treated with the ER stress inducers tunicamycin or brefeldin A for 24 hours. Microarray analysis was used to determine changes in gene expression associated with the induction of ER stress, and to compare this induction in wildtype, p53 knockout or DICER mutant HCT116 colon cancer cells Triplicate samples of HCT116 wildtype, HCT116 p53 knockout and HCT116 DICEREX5/EX5 cells were treated with with 0.5 mg/ml of BFA or 2 mg/ml of Tm for 24 h. Following treatment, cells were harvested and lysed in TRIzol reagent and RNA was extracted. Microarray analysis was carried out using Affymetrix HG-U133_Plus-2 arrays.

2015-04-01 | E-GEOD-63252 | biostudies-arrayexpress

Expression profiling of HCT116 cells transfected with shCTRL or shKSR1

Project description:We engineered HCT116 cells by transfecting a non targeting control hairpin or 2 different short hairpin against KSR1 to knockdown KSR1 and microarrays were performed on non-transfected controls, non-targeting shRNA controls, shRNA #1 targeting KSR1, and shRNA #2 targeting KSR1. We used microarray for molecular profiling of colon cancer cells in presence or in absence of KSR1, an important scaffold of Raf/MEK/ERK pathway and identify genes which are regulated by KSR1 Cell lines were measured in as single biological replicates 1. HCT116 untransfected 2 HCT116 + shCTRL 3.HCT116 + shKSR1#1 4. 3.HCT116 + shKSR1#2

2015-01-28 | E-GEOD-65351 | biostudies-arrayexpress

HCT116 (CRC): control siRNA vs. ZNF746 siRNA Transfected

Project description:Transcriptional profiling of HCT116 cells compared to untreated control with HCT116 cells transfected with ZNF746 siRNA plasmid. Goal was to determine the effects of ZNF746 gene transfection on CRC progression. Two-condition experiment, HCT116 vs. ZNF746 siRNA.

2019-12-01 | GSE90832 | GEO

Identification of genes involved in RAS oncogenic activity in human colorectal cancer cell line HCT116

Project description:The study aimed to identify genes essential for the maintenance of the transformed phenotype of the colorectal cancer cell line HCT116, which is dependent on the continued expression of the activated KRAS oncogene (KRASG13D). We generated HCT116 cell lines stably expressing an inducible shRNA-expressing retroviral vector targeting KRAS (Ngo et al., Nature, 2006). In cells engineered to express the bacterial tetracycline repressor, the shRNA is expressed specifically upon doxycycline addition. With this system, we showed that inducible down-regulation of KRAS is triggering cell death in the HCT116 cells, suggesting oncogene addiction in this cell line. In this study, we compared the gene expression profile of HCT116 cells where KRAS has been downregulated for different lengths of time, aiming at identifying RAS-target genes. We also compared the gene expression profile of the parental HCT116 cell line with two derived isogenic cell lines, Hke3 and Hkh-2, where the activated KRAS gene has been deleted by homologous recombination.

2022-04-03 | GSE199871 | GEO

The RALA pathway can maintain the proliferation of KRAS- and BRAF-mutated cancer cells

Project description:By silencing of RALA, a downstream member of the RAS signal transduction pathway, we aimed to determine whether genes downstream of a mutated KRAS (codon 12 or 13) or a mutated BRAF can have significant functions in colorectal cancer carcinogenesis. RALA was silenced in three colorectal cancer cell lines (SW480, HCT116 and HT29). Effects were normalized to mock-transfected cells and the effects of scramble siRNA were excluded. SW480, HCT116 and HT29 cell lines were treated with the PI3K inhibitor LY294002 or DMSO.

2015-06-20 | E-GEOD-39857 | biostudies-arrayexpress