Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Global Gene expression profile of Phorone exposed to Chemically Transformed C3H10T1/2 cells.

ABSTRACT: In this study, we have investigated the changes in transformed cells that occur after GSH depletion and may be critical to accentuate the attenuation of carcinogenesis. The in vitro carcinogenesis method and GSH depletor Phorone (PHO) were used. We found that exposure of transformed C3H10T1/2 cells to PHO (2mM) caused attenuation of transformed cell growth as seen in soft agar assay. Loss of cellular GSH content, increase in intracellular ROS generation, and DNA strand break formation also occurred. A microarray based study using 8x60k oligonucleotide array in duplicate revealed changes in global gene expression profile. Our study has identified changes in expression of many genes that may contribute in abatement of carcinogenesis.

ORGANISM(S): Mus musculus

PROVIDER: GSE46469 | GEO | 2016/04/30

SECONDARY ACCESSION(S): PRJNA200576

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Diethyl maleate inhibits MCA+TPA transformed cell growth via modulation of GSH, MAPK, and cancer pathways

Project description:Murine or human cancer cells have high glutathione levels. Depletion of the elevated GSH inhibits proliferation of cancer cells. Molecular basis for this observation is little understood. In an attempt to find out the underlying mechanism, we reproduced these effects in transformed C3H10T1/2 and BALB/c 3T3 cells using diethyl maleate and studied cytogenomic changes in the whole mouse genome using spotted 8 × 60K arrays. Transformed cells revealed an increase in GSH levels. GSH depletion by DEM inhibited the growth of transformed cells. The non-cytotoxic dose of DEM (0.25 mM) resulted in GSH depletion, ROS generation, cell cycle arrest, apoptosis, decrease in anchorage independent growth, gene expression changes and activation of all three members of the MAPK family. Increase in intracellular GSH levels by GSHe countered the effect of DEM. These results support the physiological importance of GSH in regulation of gene expression for transformed cell growth restraint. This study is of interest in not only understanding the molecular biology of the transformed cells, but also in identifying new targets for development of gene therapy together with the chemotherapy.

2014-06-02 | GSE44650 | GEO

Diethyl maleate inhibits MCA+TPA transformed cell growth via modulation of GSH, MAPK, and cancer pathways

Project description:Murine or human cancer cells have high glutathione levels. Depletion of the elevated GSH inhibits proliferation of cancer cells. Molecular basis for this observation is little understood. In an attempt to find out the underlying mechanism, we reproduced these effects in transformed C3H10T1/2 and BALB/c 3T3 cells using diethyl maleate and studied cytogenomic changes in the whole mouse genome using spotted 8 M-CM-^W 60K arrays. Transformed cells revealed an increase in GSH levels. GSH depletion by DEM inhibited the growth of transformed cells. The non-cytotoxic dose of DEM (0.25 mM) resulted in GSH depletion, ROS generation, cell cycle arrest, apoptosis, decrease in anchorage independent growth, gene expression changes and activation of all three members of the MAPK family. Increase in intracellular GSH levels by GSHe countered the effect of DEM. These results support the physiological importance of GSH in regulation of gene expression for transformed cell growth restraint. This study is of interest in not only understanding the molecular biology of the transformed cells, but also in identifying new targets for development of gene therapy together with the chemotherapy. Agilent one-color experiment; Organism: Mus musculus; Agilent Custom Mouse Whole Genome Mouse 8x60k gene expression designed by Genotypic Technology Private Limited; Labeling kit: Agilent Quick-Amp labeling Kit (p/n5190-0442).

2014-06-02 | E-GEOD-44650 | biostudies-arrayexpress

c3h10t1/2 with dexamethasone

Project description:determine genes regulated by dexamethasone in c3h10t1/2 cells after 90 minutes of treatment compared to vehicle Keywords: treatment comparison microarray c3h10t1/2 cells were treated with vehicle or 1uM dexamethasone for 90 minutes (3 biological replicates of each) RNA samples were isolated from RNeasy kit (Qiagen) hybridized all samples to a pool of RNA from vehicle and treated c3h10t1/2 cells

2010-05-25 | E-GEOD-10900 | biostudies-arrayexpress

ERK activation, gene dysregulations and cell transformation at submicromolar doses of Cr6+ in C3H10T1/2 and BALB/c 3T3 cells: interaction with Lipoic acid

Project description:The molecular mechanism of Cr6+ carcinogenicity is not well understood. Studies advocate a key involvement of the altered cytogenomics and dysregulated pathways in Cr6+ toxicity. However, the dissimilarity in expression of genes and pathways in cells transformed by Cr6+ has led us to supplement more data on the subject. We report here genomics of cells transformed after acute exposure to submicromolar (0.01or1ÂµM) test doses of Cr6+; the non-cytotoxic submicromolar test concentrations transformed the mammalian cells; the characteristic gain of anchorage independent growth potential was demonstrable in soft agar assay. C3H10T1/2 and BALB/c 3T3 cell transformation assay has been used which is established in literature as the in vitro carcinogenesis test system. Gene expression profile of the transformed cells was found to be dysregulated at both the toxicant doses. PARP1 gene was significantly up regulated and SFN, MTIF2, IRGQ, RAVER2, SLC2A6, MLLT3, EPB4.1L3, JAK1, RALGPS1, EXTL3, PRMT6, PREB, SERPINE1, MORC4 genes were significantly down regulated commonly at two test concentrations. These genes were found to be involved in tumour suppression, DNA repair, cell cycle control, energy metabolism and biosynthesis.Cr6+ also induced MAPK signalling via ERK phosphorylation. Activation of ERK signalling, dysregulation of gene expressions, and cell transformation was prevented by alpha lipoic acid (LA) in equimolar concentrations. The acute exposure to submicromolar concentrations of Cr6+ can induce cell transformation and gene dysregulations in mammalian cell. The influenced genes are crucial for progression of Cr6+ toxicity and their mitigation by LA shows critical role of redox reactions in Cr6+ toxicity. Agilent one-color experiment,Organism: Mus musculus ,Agilent-Whole Genome Mouse 4x44k (AMADID: 14868) , Labeling kit: Agilent Quick-Amp labeling Kit (p/n5190-0442) C3H10T1/2 cells treated with 1uM or 0.01uM Cr(V1)

2015-12-31 | E-GEOD-43156 | biostudies-arrayexpress

c3h10t1/2 with dexamethasone

Project description:determine genes regulated by dexamethasone in c3h10t1/2 cells after 90 minutes of treatment compared to vehicle Keywords: treatment comparison microarray

2008-03-21 | GSE10900 | GEO

Mkx overexpression effect in C3H10T1/2 cells

Project description:Analysis of C3H10T1/2 cells overexpressing Mkx. This microarray results show that Mkx has the potential ability to promote differentiation to tendon, ligament and annulus fibrosus cells.

2016-05-11 | GSE81276 | GEO

Expression data from C3H10T1/2 cells treated with 3.3 nM BMP7 vs vehicle

2015-07-21 | GSE71101 | GEO

ERK activation, gene dysregulations and cell transformation at submicromolar doses of Cr6+ in C3H10T1/2 and BALB/c 3T3 cells: interaction with Lipoic acid

Project description:The molecular mechanism of Cr6+ carcinogenicity is not well understood. Studies advocate a key involvement of the altered cytogenomics and dysregulated pathways in Cr6+ toxicity. However, the dissimilarity in expression of genes and pathways in cells transformed by Cr6+ has led us to supplement more data on the subject. We report here genomics of cells transformed after acute exposure to submicromolar (0.01or1µM) test doses of Cr6+; the non-cytotoxic submicromolar test concentrations transformed the mammalian cells; the characteristic gain of anchorage independent growth potential was demonstrable in soft agar assay. C3H10T1/2 and BALB/c 3T3 cell transformation assay has been used which is established in literature as the in vitro carcinogenesis test system. Gene expression profile of the transformed cells was found to be dysregulated at both the toxicant doses. PARP1 gene was significantly up regulated and SFN, MTIF2, IRGQ, RAVER2, SLC2A6, MLLT3, EPB4.1L3, JAK1, RALGPS1, EXTL3, PRMT6, PREB, SERPINE1, MORC4 genes were significantly down regulated commonly at two test concentrations. These genes were found to be involved in tumour suppression, DNA repair, cell cycle control, energy metabolism and biosynthesis.Cr6+ also induced MAPK signalling via ERK phosphorylation. Activation of ERK signalling, dysregulation of gene expressions, and cell transformation was prevented by alpha lipoic acid (LA) in equimolar concentrations. The acute exposure to submicromolar concentrations of Cr6+ can induce cell transformation and gene dysregulations in mammalian cell. The influenced genes are crucial for progression of Cr6+ toxicity and their mitigation by LA shows critical role of redox reactions in Cr6+ toxicity.

2015-12-31 | GSE43156 | GEO

microRNA expression in C3H10T1/2 cells treated with BMP7 vs vehicle

Project description:Multipotent C3H10T1/2 cells can be induced to differentiate into mature brown adipocytes by 3-days BMP7 pretreatment followed by standard adipogenic induction. In this study, we used microRNA array to identify the microRNAs that were regulated by 3-days BMP7 treatment in C3H10T1/2 cells. One BMP7-treated sample and one vehicle-treated sample were used in this study to obtain the fold expression of microRNAs between BMP7 vs vehicle.

2015-07-22 | E-GEOD-71157 | biostudies-arrayexpress

microRNA expression in C3H10T1/2 cells treated with BMP7 vs vehicle

Project description:Multipotent C3H10T1/2 cells can be induced to differentiate into mature brown adipocytes by 3-days BMP7 pretreatment followed by standard adipogenic induction.

2015-07-22 | GSE71157 | GEO

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