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Differential expression of proteins due to Cobalt(II) Chloride induced pseudohypoxia in Jurkat cells

ABSTRACT: To demonstrate the mechanisms underlying Cobalt(II) Chloride driven pseudohypoxia, proteomic dysregulations were studied in a human T-cell Lymphoma cell line (Jurkat). This proteomics data generated the abundance ratios of proteins in CoCl2 treated versus untreated Jurkat cells. Concisely, Jurkat cells were treated with CoCl2 (50uM) in complete RPMI media. Tryptic digested and desalted peptide samples were injected in Thermoscientific Q-Exactive Plus instruments through EasyNLC HPLC autosampler. The instruments were set to MS1 resolution of 70000 and MS2 resolution of 17500. The acquisition experiments were optimized to run on 2 hours gradients. The MS spectra were analyzed using the Thermoscientific mass informatics platform Proteome discoverer version 2.2. The common workflows for discovery proteomics were used with Mascot and SequestHT. This dataset assisted in identifying the pseudohypoxia-driven changes in lymphoma progression and revealed many druggable targets in the context of metastasis in T-cell malignanices.

INSTRUMENT(S): Q Exactive Plus

ORGANISM(S): Homo Sapiens (ncbitaxon:9606)

SUBMITTER: Rahul Purwar

PROVIDER: MSV000095681 | MassIVE | Fri Aug 23 09:16:00 BST 2024

SECONDARY ACCESSION(S): PXD055142

REPOSITORIES: MassIVE

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Project description:We examined the biological effects of a potent second-generation proteasome inhibitor, ixazomib, in T-cell lymphoma and Hodgkin lymphoma cell lines and human xenograft models. Ixazomib resulted in time- and dose-dependent cytotoxicity and apoptosis in all cell lines (IC50’s <75nM). In vivo studies via SCID tumor xenografts showed significant inhibition of tumor growth (P<0.001) with significantly improved survival (P<0.001) in Jurkat and L540 models with ixazomib-treated mice versus controls. Through global transcriptome and network analyses, ixazomib-treated Jurkat and L540 cells showed significant overlap in biological functions involved in regulation of cell cycle, chromatin modification, and DNA repair processes with a lack of conservation observed in a relatively ixazomib-resistant cell line, L428. Moreover, the predicted activation and inhibition status of tumor suppressors and oncogenes strongly favored ixazomib inhibition of tumor progression. Most notably, ixazomib down-regulated protein levels of MYC and its target genes. Additionally, chromatin immunoprecipitation showed that histone H3 acetylation affected MYC levels and cell death response to ixazomib. Furthermore, inhibition of MYC with JQ1 resulted in synergistic cell death in L428, which was confirmed utilizing MYC knockout. Collectively, ixazomib down-regulated MYC and downstream substrates in TCL and HL, while resistance appeared mediated through MYC- and CHK1-dependent mechanisms. Jurkat (TCL)and L540 cells were treated with ixazomib for 24 hours, RNA was isolated using RNeasy Minikit (Qiagen), following instructions recommended supplied by the manufacturer. Purity and the yield of isolated RNA was determined using Bioanalyzer. These experiments were performed in biological triplicates. Microarray experiment with Jurkat and L540 was performed Affy Human Gene Chip 2.0, at UMASS Medical School Genomic Core facility. Data for Jurkat and L540 cell lines were background adjusted and quantile normalized using RMAExpress. Statistically relevant genes were determined by applying LIMMA with a FDR < 0.05 that resulted in 764 significant genes for the Jurkat experimental group and 5819 significant genes for the L540 experimental group.

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Differential expression of proteins due to Cobalt(II) Chloride induced pseudohypoxia in Jurkat cells

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