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YM155 targets CMS1 colorectal cancer

ABSTRACT: Multi-omics integration identifies a selective vulnerability of colorectal cancer molecular subtypes to YM155

PROVIDER: PRJEB27582 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR2679240.fastq.gz	Fastqsanger.gz
	ERR2679241.fastq.gz	Fastqsanger.gz
	ERR2679234.fastq.gz	Fastqsanger.gz
	ERR2679235.fastq.gz	Fastqsanger.gz
	ERR2679236.fastq.gz	Fastqsanger.gz

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

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. We performed expression profiling experiments in order to validate molecular subtypes for selected cell lines

2018-07-03 | GSE116528 | GEO

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

2018-07-03 | GSE116529 | GEO

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

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

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

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

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YM155 treated KYSE410

Project description:We used microarrays to detail the gene expression profiles of KYSE410 cell line to identify distinct up and down-regulated genes during treatment with cisplatin. KYSE410 cell line were treated with 20 nM YM155 for 6 hrs and selected for RNA extraction and hybridization on Affymetrix microarrays. We sought to gene expression profiles of KYSE 410 cell line treated with cisplatin.

2015-01-16 | E-GEOD-65009 | biostudies-arrayexpress

Matrisome-focused integrative omics analysis reveals stromal phenotypes associated with consensus molecular subtypes in colorectal cancer

Project description:Matrisome-focused integrative omics analysis reveals stromal phenotypes associated with consensus molecular subtypes in colorectal cancer This reseaerch is conducted using colorectal cancer. TMT 11plex experiment

2022-10-27 | MSV000090604 | MassIVE

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.

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Project description:EZH2 inhibitors have been developed to treat certain cancers. To maximize the anticancer acttivity of EZH2 inhibition, we combined an EZH2 inhibitor EPZ6438 with YM155, which leads to dramatic cell death. We used microarrays to detail the global gene expression profiles.

2023-01-13 | GSE208593 | GEO

RNA-Seq of YM155 treated KMB7 wild-type and SLC35F2 knock-out cells

Project description:SLC35F2 was identified as a transporter of DNA damage inducing agent YM155. We then did a comparative transcriptomics experiment comparing wild-type and SLC35F2 knock-out KBM7 cells.

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Expression profiling of colorectal cancer cell lines.

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