Mus musculus
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ABSTRACT:
PROVIDER: PRJNA184732 | ENA |
REPOSITORIES: ENA
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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. 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
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
Project description:Investigation of the transcription profile of cells transformed by Cr6+ in vivo was undertaken. The objective was to elucidate genomic changes underlying the mechanism of action of the carcinogenic dose of Cr6+and their prevention using metabolic antioxidant Lipoic acid (LA). Cr6+ was administered intraperitoneally to LPS+TPA challenged Swiss albino mice in host mediated cell transformation assay using peritoneal macrophages in vivo. The cell transforming potential of Cr6+ test doses was validated by gain of anchorage independent growth potential in soft agar and loss of Fc receptor on target cells. LA was administered in equimolar doses. Compared to non-transformed cells, the gene expression profile of transformed cells was found to be dysregulated substantially and in dose dependent manner. Genes showing down regulation were found to be involved in tumour suppression; apoptosis, DNA repair, and cell-cycle. A similar response was noted in the genes pertaining to immune system, morphogenesis, cell-communication, energy-metabolism, and biosynthesis. The co-administration of lipoic acid prevented the transcription dysregulation and cell transformation by Cr6+ in vivo. The influenced pathways seem to be crucial for progression as well as mitigation of Cr toxicity; and their response to LA indicated their critical role in mechanism of anti-carcinogenic action of LA. Results are of importance to mitigate Cr6+ induced occupational cancer hazard.
2013-05-01 | GSE41419 | GEO
Project description:Investigation of the transcription profile of cells transformed by Cr6+ in vivo was undertaken. The objective was to elucidate genomic changes underlying the mechanism of action of the carcinogenic dose of Cr6+and their prevention using metabolic antioxidant Lipoic acid (LA). Cr6+ was administered intraperitoneally to LPS+TPA challenged Swiss albino mice in host mediated cell transformation assay using peritoneal macrophages in vivo. The cell transforming potential of Cr6+ test doses was validated by gain of anchorage independent growth potential in soft agar and loss of Fc receptor on target cells. LA was administered in equimolar doses. Compared to non-transformed cells, the gene expression profile of transformed cells was found to be dysregulated substantially and in dose dependent manner. Genes showing down regulation were found to be involved in tumour suppression; apoptosis, DNA repair, and cell-cycle. A similar response was noted in the genes pertaining to immune system, morphogenesis, cell-communication, energy-metabolism, and biosynthesis. The co-administration of lipoic acid prevented the transcription dysregulation and cell transformation by Cr6+ in vivo. The influenced pathways seem to be crucial for progression as well as mitigation of Cr toxicity; and their response to LA indicated their critical role in mechanism of anti-carcinogenic action of LA. Results are of importance to mitigate Cr6+ induced occupational cancer hazard. Agilent one-color experiment, Organism: Mus musculus, Agilent-Whole Genome Mouse 4x44k (AMADID: 14868), Labeling kit: Agilent Quick-Amp labeling Kit (p/n5190-0442)
2013-05-01 | E-GEOD-41419 | biostudies-arrayexpress
Project description:Lipoic acid prevents Cr6+ induced cell transformation and the associated genomic dysregulation.
| PRJNA176924 | ENA
Project description:miRNA array of a timecourse of 3T3-L1 differentiating into white adipocytes and C3H10T1/2 into brown adipocytes
2016-12-31 | GSE75697 | GEO
Project description:The gene mucAB has an error-prone activity in bacteria. We introduced mucAB into mouse 3T3 cells with an expression vector and found drastic increase of spontaneous transformation, accompanied by increase of expression of eight oncogenes, i. e., Gpnmb, Foxml, Maff, Myc, Aurka, Aukb, Fosl1, and Anxa8 and decrease of expression in two oncogenes, i. e., Lrig1 and RhoX in order of the magnitude of change, as compared with those in non-treated 3T3 cells. Transformation of cultured mouse BALB 3T3 cells was used as an indicator of cellular oncogenesis. We examined effects of introduction of foreign bacterial plasmid gene into mouse cells on spontaneous transformation frequency, accompanied by change of expression of known oncogenes. To do this, 3T3 cells with or without mucAB were compared for expression of known genes, using the microarray method.
2013-12-01 | E-GEOD-42927 | biostudies-arrayexpress
Project description:Genome wide lncRNA and mRNA expression profiling at day 0 and day 4 after induction of adipocyte differentiation in C3H10T1/2 and 3T3-L1 cells were analyzed by Arraystar Mouse LncRNA Microarray V3.0
2021-12-15 | GSE190733 | GEO
Project description:C3H10T1/2 stem cells are committed to the adipocyte lineage by treatment with BMP-4 and grown to postconfluence. When subjected to our standard differentiation protocol, the committed cells differentiate into adipocytes in a manner indistinguishable from that of 3T3-L1 preadipocytes. In contrast, C3H10T1/2 cells not committed with BMP-4 remain undifferentiated despite treatment with differentiation inducers. The molecular basis of the commitment process, however, has not been elucidated. Since postconfluent uncommitted and committed C3H10T1/2 cells respond differently to the differentiation inducers, it was reasoned that the two cell types differed at the gene expression level. Therefore, we undertook microarray gene expression profiling to detect changes between the two cell populations at postconfluence to identify expressed genes that may be responsible for the dramatic change in phenotype. Keywords: control vs treated
2007-09-26 | GSE5921 | GEO
Project description:C3H10T1/2 stem cells are committed to the adipocyte lineage by treatment with BMP-4 and grown to postconfluence. When subjected to our standard differentiation protocol, the committed cells differentiate into adipocytes in a manner indistinguishable from that of 3T3-L1 preadipocytes. In contrast, C3H10T1/2 cells not committed with BMP-4 remain undifferentiated despite treatment with differentiation inducers. The molecular basis of the commitment process, however, has not been elucidated. Since postconfluent uncommitted and committed C3H10T1/2 cells respond differently to the differentiation inducers, it was reasoned that the two cell types differed at the gene expression level. Therefore, we undertook microarray gene expression profiling to detect changes between the two cell populations at postconfluence to identify expressed genes that may be responsible for the dramatic change in phenotype. Experiment Overall Design: C3H10T1/2 cells were plated and treated with 50 ng/ml BMP4 and grown to postconfluence. Control samples were treated in the same manner were not given BMP4. Total RNA was collected at postconfluence. There were 3 replicates each for control and treated cells.
2008-06-14 | E-GEOD-5921 | biostudies-arrayexpress