Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The mRNA profile of HT29 cells after treatment with YM155

ABSTRACT: To investigate the molecular mechanisms by which YM155, a survivin inhibitor, suppresses tumor progression, HT29 human colon cancer cells were treated with YM155 for 24 hours. The aim was to elucidate how YM155 affects the expression of various cancer-related genes, including survivin.

ORGANISM(S): Homo sapiens

PROVIDER: GSE298631 | GEO | 2026/06/22

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNAseq of CD4 T cells treated with survivivin inhibitor YM155 for 72h

Project description:CD4 T cells from 4 healthy women were activated with aCD3 and treated with the survivin inhibitor YM155, 10 ng/ml or control during 72 hours. The last 2 hours with upplement of IFNg. The objective was to understand the action of survivin (coded by BIRC5 gene) in CD4 T cells.

2022-11-29 | GSE190351 | GEO

RNAseq of CD4 T cells treated with survivivin inhibitor YM155 for 24h

Project description:CD4 T cells from 4 healthy women were activated with aCD3 and treated with the survivin inhibitor YM155, 10 ng/ml or control during 24 hours. The last 2 hours with upplement of IFNg. The objective was to understand the action of survivin (coded by BIRC5 gene) in CD4 T cells.

2022-11-29 | GSE190352 | GEO

The mRNA profile of HT29 cells after treatment with YM155

Project description:The mRNA profile of HT29 cells after treatment with YM155

| PRJNA1270057 | ENA

Consensus Molecular Subtype predicts differential vulnerability of colorectal cancer to the survivin suppressant YM155 I

Project description:Tumor heterogeneity is a major challenge to the treatment of colorectal cancer (CRC). Recently, a transcriptome-based classification was developed, segregating CRC into four consensus molecular subtypes (CMS) with distinct biological and clinical characteristics. Here, we applied the CMS classification on CRC cell lines to identify novel subtype-specific drug vulnerabilities. We combined publicly available transcriptome data from multiple resources to assign 159 CRC cell lines to CMS. By integrating results from large scale drug screens, we discovered that CMS1 cancer is highly vulnerable to the survivin suppressor YM155. We confirmed our results using an independent panel of CRC cell lines and demonstrate a 100-fold higher sensitivity of CMS1 lines. This vulnerability was specific to YM155 and not observed for commonly used chemotherapeutic agents. In CMS1 cancer, low concentrations of YM155 induced apoptosis and expression signatures associated with NFkappaB and ER stress mediated apoptosis signaling. Using a genome-wide CRISPR/Cas9 screen, we discovered a novel role of genes involved in LDL-receptor recycling as modulators of YM155 response in CMS1 CRC. Our work shows that combining drug response data with CMS classification in cell lines can reveal specific vulnerabilities and propose YM155 as novel CMS1 specific drug.

2018-07-03 | GSE116529 | GEO

Consensus Molecular Subtype predicts differential vulnerability of colorectal cancer to the survivin suppressant YM155 II

2018-07-03 | GSE116528 | GEO

Drug-induced mitochondrial oxidative stress is responsible for various effects of the survivin inhibitor Sepantronium Bromide (YM155) in triple negative breast cancer cells

Project description:Sepantronium bromide (YM155), a transcriptional inhibitor of anti-apoptotic protein survivin, is considered as a potential drug candidate for triple negative breast cancers (TNBC). Regardless of its excellent performance in pre-clinical models of TNBC, in patients, this drug was unable to outperform the standard chemotherapy docetaxel. The goal of this study was to identify the pathways/molecules affected by YM155 in TNBC cell lines. Detailed biochemical analysis of the paired YM155-sensitive and resistant cell lines indicates that induction of mitochondrial oxidative stress is a first-line response to the drug, ultimately leading to growth inhibition and induction of cell death. Multiple pathways involved in dampening oxidative stress-induced damages are differentially regulated in YM155-resistant cells. Furthermore, the emergence of YM155 resistance is associated with an extensive transcriptional reprogramming and alteration of many more biological pathways in addition to those identified by biochemical assays. Molecules associated with these biological pathways will potentially serve as biomarkers predicting YM155 sensitivity in TNBC cells.

2020-10-24 | GSE139364 | GEO

Transcriptome analysis of novel CPT-CEF-treated HT29 colon cancer cells to evaluate drug cytotoxicity

Project description:Purpose: To identify differentially expressed genes in HT29 colon cancer cells after treatment with a novel formulation of camptothecin with β-cyclodextrin-EDTA-Fe3O4 nanoparticle-conjugated nanocarriers (CPT-CEF) Methods:Treated HT29 cell lines with CPT-CEF, isolated total RNA from HT29 colon cancer cells, and prepared library for RNA sequencing. Carried out comparative transcriptomic studies between treated and untreated cells to find out which gene functions were dysregulated by CPT-CEF. Results: The study yielded 247 DEGs ((FDR<0.05, FC>2.0) that were affected by CPT-CEF treatment in the HT29 colon cancer cells. The results obtained from cell cycle analysis, mitochondrial depolarization assay and acridium orange/propidium iodide double staining showed potential of CPT-CEF in cancer cell inhibition. Conclusion: Our study successfully identified DEGs in the CPT-CEF treated HT29 colon cancer cells that pointed to inhibition of cancer progression. To further affirm, animal studies are needed.

2021-09-15 | GSE165875 | GEO

Diverse effect of WWOX overexpression in HT29 colon cancer cell line.

Project description:The WWOX gene is a tumor suppressor probably involved in regulation of cell cycle and apoptosis and downregulated in variety of cancer types.However, its role in colon cancerogenesis is unknown. The aim of this study was to characterize how WWOX may be involved in colon cancerogenesis or cancer progression, how it influences the basic cancer cell features and modifies cell expression profile.Our observations suggest that in HT29 colon cancer cell line increased expression of WWOX may result in transition of cancer cells into more normal- like colon epithelium phenotype, on the other hand in SW480 WWOX revealed the well-known tumour suppressor properties. However, as the colon cancer is very heterogeneous disease, obtained discrepancies may reflect the known differences between cell lines and cancerogenesis pathway, which they undergone. HT29 colon cancer cells were stably transfected with WWOX cDNA. HT29 cells transfected with an empty vector served as a control. Total mRNA was isolated to look for gene-expression differences induced by the WWOX overexpression.

2014-01-23 | E-GEOD-54298 | biostudies-arrayexpress

ERbeta modulation of NFkB pathway in colon cancer cell lines SW480 and HT29

Project description:Analysis of differentially expressed genes in colon cancer cell lines SW480 and HT29 with and without stably expressed ERbeta gene, with and without 10ng/mL TNFa treatment for 2 and 24 hours. Total RNA obtained from colon cancer cell lines SW480 and HT29 with and without stably expressed ERbeta gene, with and without 10ng/mL TNFa treatment for 2 and 24 hours.

2016-07-17 | E-GEOD-65979 | biostudies-arrayexpress

Gene expression profiles of HT29 cells in which REG4 expression was suppressed.

Project description:GATA6 is a zinc finger transcription factor that is required for the proliferation, development and specific gene regulation in the gastrointestinal tract. We have recently reported that GATA6-mediated induction of the intestinal stem cell marker LGR5 is required for the tumorigenicity of colon cancer cells. However, knockdown of LGR5, unlike GATA6, does not affect the proliferation of these cells under adherent conditions. Here we show that REG4, a member of the regenerating islet-derived (REG) family, is a target of GATA6. We further demonstrate that REG4 is downregulated by overexpression of miR-363, which suppresses GATA6 expression. Moreover, we show that GATA6-mediated activation of REG4 causes an acceleration of the growth of colon cancer cells under adherent conditions. These results suggest that GATA6 simultaneously activates the transcription of genes required for growth (REG4) and clonogenicity (LGR5), and the miR-363-GATA6-REG4/LGR5 pathway is critical for colorectal tumorigenesis. HT29 cells were transfected with a siRNA targeting REG4.

2016-06-15 | E-GEOD-62318 | 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