Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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GSK-inhibitor treatment in IMR32 neuroblastoma cell line

ABSTRACT: Cells were cultured in RPMI 1640 (Gibco), supplemented with 10% fetal bovine serum (FBS) (Gibco), 2mM L-glutamine (Gibco) and 1% Penicillin-Streptomycin solution (Gibco). IMR32 cells were treated as follows; untreated control, 24h 1uM azakenpaullone, 24h 1uM BIO or 24h 28mM LiCl with biological duplicates.

INSTRUMENT(S): Illumina Genome Analyzer IIx

ORGANISM(S): Homo sapiens

SUBMITTER: Thomas Schwarzl

PROVIDER: E-MTAB-1684 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Although the consequences of genotoxic injury include cell cycle arrest and apoptosis, cell survival responses after genotoxic injury can produce intrinsic death-resistance and contribute to the development of a transformed phenotype. Protein tyrosine phosphatases (PTPs) are integral components of key survival pathways, and are responsible for their inactivation, while PTP inhibition is are often associated with enhanced cell proliferation. Our aim was to elucidate signaling events that modulate cell survival after genotoxin exposure. Diploid human lung fibroblasts (HLF) were treated with Cr(VI) (as Na2CrO4), a well known human respiratory carcinogen that induces a wide spectrum of DNA damage, in the presence and absence of a broad-range PTP inhibitor, sodium orthovanadate. Notably, PTP inhibition abrogated Cr(VI)-induced clonogenic lethality. The enhanced survival of Cr(VI)-exposed cells after PTP inhibition was predominantly due to a bypass of cell cycle arrest and was not due to decreased Cr uptake as evidenced by unchanged Cr-DNA adduct burden. Additionally, the bypass of Cr-induced growth arrest by PTP inhibition, was accompanied by a decrease in Cr(VI)-induced expression of cell cycle inhibiting genes, and an increase in the Cr(VI)-induced expression of cell cycle promoting genes. Importantly, PTP inhibition resulted in an increase in forward mutations at the HPRT locus, supporting the hypothesis that PTP inhibition in the presence of DNA damage may lead to genomic instability, via bypass of cell cycle checkpoints. Experiment Overall Design: Experimental factor was chemical treatment type (3 of them) Experiment Overall Design: (1) No: HLF 1-1, HLF 1-2, HLF 1-3, HLF 1-4 Experiment Overall Design: (2) 1uM Cr(VI): HLF 3-1, HLF 3-2, HLF 3-3, HLF 3-4 Experiment Overall Design: (3) 10uM SOV + 1uM Cr(VI): HLF 4-1, HLF 4-2, HLF 4-3, HLF 4-4 Experiment Overall Design: Biological replicates: 4 different RNA extractions from 4 different cell cultures=quadruplicate per chemical treatment type

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GSK-inhibitor treatment in IMR32 neuroblastoma cell line

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