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

The Anticancer Mechanism of the Ribonucleotide Reductase Inhibiting Drug COH29 Involves Suppression of DNA Repair

ABSTRACT: Mechanism of Action Study for COH29 Compare COH29 treatment in DNA-repair deficient cell line with truncated BRCA1 (HCC1937) versus phenotypically normal cell line with exogenous WT BRCA1 expression (HCC1937+BRCA1)

ORGANISM(S): Homo sapiens

SUBMITTER: Charles Warden

PROVIDER: E-GEOD-55004 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

The Novel Ribonucleotide Reductase Inhibitor COH29 Inhibits DNA Repair In Vitro.

Chen Mei-Chuan MC Zhou Bingsen B Zhang Keqiang K Yuan Yate-Ching YC Un Frank F Hu Shuya S Chou Chih-Ming CM Chen Chun-Han CH Wu Jun J Wang Yan Y Liu Xiyong X Smith D Lynne DL Li Hongzhi H Liu Zheng Z Warden Charles D CD Su Leila L Malkas Linda H LH Chung Young Min YM Hu Mickey C-T MC Yen Yun Y

Molecular pharmacology 20150326 6

COH29 [N-(4-(3,4-dihydroxyphenyl)-5-phenylthiazol-2-yl)-3,4-dihydroxybenzamide], a novel antimetabolite drug developed at City of Hope Cancer Center, has anticancer activity that stems primarily from the inhibition of human ribonucleotide reductase (RNR). This key enzyme in deoxyribonucleotide biosynthesis is the target of established clinical agents such as hydroxyurea and gemcitabine because of its critical role in DNA replication and repair. Herein we report that BRCA-1-defective human breast ...[more]

PMID: 25814515

Similar Datasets

The Anticancer Mechanism of the Ribonucleotide Reductase Inhibiting Drug COH29 Involves Suppression of DNA Repair

Project description:Mechanism of Action Study for COH29

2015-05-08 | GSE55004 | GEO

Integration of BRCA1-mediated miRNA and mRNA signatures reveal miR-146a, miR-99b and miR-205 regulation of the TRAF2 and NFkB pathways (mRNA dataset)

Project description:BRCA1 deregulation is a frequent event in the pathogenesis of breast as well as other cancers. In addition to the DNA repair functions of BRCA1, it is involved in a wide range of cellular processes such as cell cycle, chromatin remodeling or transcription. However, the molecular events underlying BRCA1-associated tumorigenesis are still largely unknown. In order to deepen our understanding of BRCA1-associated tumorigenesis, we integrated data from mRNA and miRNA microarray experiments on the HCC1937 breast cancer cell line, and the isogenic HCC1937 stably expressing BRCA1, to obtain significant miRNA-mRNA relationships associated to the presence of the BRCA1 gene. Our results demonstrate that integration of mRNA and miRNA associated to BRCA1 expression was useful to discover new miRNA-gene interactions as molecular events underlying BRCA1-mediated tumorigenesis. Transcriptional profiling of the BRCA1-null HCC1937 cell line and HCC1937 cells after stable transfection of BRCA1. Two-condition experiment: Universal Human Reference RNA (Stratagene, catalog #740000) (Cy3) vs. cell line (Cy5). Biological replicates: 3 HCC1937, 3 BRCA1-transfected HCC1937 cells.

2011-12-24 | E-GEOD-30821 | biostudies-arrayexpress

Methylation profiling of ten breast cancer cell lines to identify new targets for basal-like breast cancers

Project description:In order to identify new targets for basal-like breast cancers, we performed Methyl-Seq of 10 breast cancer cell lines. Basal-like cell lines (MDAMB231, MDAMB436, HCC1937, SUM149, SUM1315 and MCF10A) were compared to luminal cell lines (MCF7 and T47D). Moreover we could also study BRCA1 influence on methylome of basal-like breast cancer. 4 of our cell lines are indeed BRCA1 mutated (MDAMB436, HCC1937, SUM149 and SUM1315) and we also developed 2 cell lines that come from the BRCA1 mutated SUM1315 cell line stably transfected with empty LXSN plasmid (SUM1315-LXSN) or with a BRCA1 coding plasmid (SUM1315-BRCA1).

2017-02-14 | E-MTAB-5468 | biostudies-arrayexpress

RNASeq of ten human breast cancer cell lines

Project description:In order to identify new targets for basal-like breast cancers, we performed RNA-Seq of 10 breast cancer cell lines. Basal-like cell lines (MDAMB231, MDAMB436, HCC1937, SUM149, SUM1315 and MCF10A) were compared to luminal cell lines (MCF7 and T47D). Moreover we could also study BRCA1 influence on transcriptome of basal-like breast cancer. 4 of our cell lines are indeed BRCA1 mutated (MDAMB436, HCC1937, SUM149 and SUM1315) and we also developed 2 cell lines that come from the BRCA1 mutated SUM1315 cell line stably transfected with empty LXSN plasmid (SUM1315-LXSN) or with a BRCA1 coding plasmid (SUM1315-BRCA1).

2017-02-14 | E-MTAB-5465 | biostudies-arrayexpress

Integration of BRCA1-mediated miRNA and mRNA signatures reveal miR-146a, miR-99b and miR-205 regulation of the TRAF2 and NFkB pathways (mRNA dataset)

2011-12-24 | GSE30821 | GEO

Integration of BRCA1-mediated miRNA and mRNA signatures reveal miR-146a, miR-99b and miR-205 regulation of the TRAF2 and NFkB pathways (miRNA dataset)

Project description:Microarray‐based techniques are being used to obtain miRNA and gene expression signatures associated with different samples. In order to deepen our understanding of BRCA1-associated tumorigenesis, we integrated data from microarray experiments to obtain significant miRNA-mRNA relationships associated with the presence of the BRCA1 gene. We obtained significant miRNA-gene-pathway relationships underlying the array signatures. Furthermore, we have demonstrated that miR-146a, miR-99b and miR-205, induced in HCC1937 BRCA1-expressing cells, commonly regulate the TRAF2 gene, a key regulator of NF-κB and MAPK pathways. In addition, re-expression of miR-146a, miR-99b or miR-205 in HCC1937 BRCA1-null cells was sufficient to modulate NF-κB activity. Thus, integration between miRNA-mRNA expression data allowed us to define genes and pathways controlled by miRNAs induced in the context of BRCA1 expression.

2011-12-24 | GSE30763 | GEO

Integration of BRCA1-mediated miRNA and mRNA signatures reveal miR-146a, miR-99b and miR-205 regulation of the TRAF2 and NFkB pathways (miRNA dataset)

Project description:Microarray?based techniques are being used to obtain miRNA and gene expression signatures associated with different samples. In order to deepen our understanding of BRCA1-associated tumorigenesis, we integrated data from microarray experiments to obtain significant miRNA-mRNA relationships associated with the presence of the BRCA1 gene. We obtained significant miRNA-gene-pathway relationships underlying the array signatures. Furthermore, we have demonstrated that miR-146a, miR-99b and miR-205, induced in HCC1937 BRCA1-expressing cells, commonly regulate the TRAF2 gene, a key regulator of NF-?B and MAPK pathways. In addition, re-expression of miR-146a, miR-99b or miR-205 in HCC1937 BRCA1-null cells was sufficient to modulate NF-?B activity. Thus, integration between miRNA-mRNA expression data allowed us to define genes and pathways controlled by miRNAs induced in the context of BRCA1 expression. Comparison of miRNA expression profiles between two isogenic cell lines differing in BRCA1 gene expression status. Single-color experiments in a pairwise comparison design with three technical replicates per cell line.

2011-12-24 | E-GEOD-30763 | biostudies-arrayexpress

COHCAP HCT116 Mutant Comparison [expression]

Project description:Genome-wide expression and methylation differences are compared for a normal HCT116 cell line and a derived mutant with altered DNA methylation patterns. The data compares the effect of a gene mutation on genome-wide expression (and methylation). This data is being published as a technical test of utility for a novel integrative genomic algorithm (COHCAP) Keywords: parental, mutant

2013-06-08 | E-GEOD-42307 | biostudies-arrayexpress

Transgenerational Gene Expression Changes Caused by Exposing Fetal Germ Cells to Endocrine Disruptors

Project description:We treated gestating female mice with vinclozolin (VZ), bisphenol A (BPA), di-(2-ethylhexyl) phthalate (DEHP), or control oil, during the time when the prospermatogonia of the exposed fetus undergo global de novo DNA methylation. Using genome-wide assays we detected changes in transcription and DNA methylation, respectively, in fetal prospermatogonia. Our results suggest that EDs exert direct epigenetic effects in the exposed fetal germ cells, but the germline corrects against deleterious effects in the subsequent generation. Pregnant mice were administered endocrine distruptors (VZ at 100 mg/kg/day, DEHP at 750 mg/kg/day, and BPA at 0.2 mg/kg/day) startin g at 12.5 days post coitum (dpc) and tissue samples were collected at 17.5 dpc.

2015-02-18 | E-GEOD-58642 | biostudies-arrayexpress

Drosha knock-down gene expression in HSPCs

Project description:Genome-wide expression differences are compared for a normal and mutant cell line. The data compares the effect of a gene mutation on genome-wide expression. empty vector (EV), shDrosha (shDr); shDr denotes hematopoietic stem-progenitor cells (HSPCs) transduced with a short-hairpin RNA targeting the miRNA-processing enzyme Drosha

2016-07-03 | E-GEOD-47403 | 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