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Impact of SOCS1 inactivation on CAR19 antitumor activity againt Nalm6 ALL (leukemia) in NSG mice

ABSTRACT: Impact of SOCS1 inactivation on CAR19 antitumor activity againt Nalm6 ALL (leukemia) in NSG mice

PROVIDER: PRJNA647454 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12274319_1.fastq.gz	Fastqsanger.gz
	SRR12274319_2.fastq.gz	Fastqsanger.gz
	SRR12274320_1.fastq.gz	Fastqsanger.gz
	SRR12274320_2.fastq.gz	Fastqsanger.gz
	SRR12274321_1.fastq.gz	Fastqsanger.gz

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Impact of SOCS1 inactivation on CAR19 antitumor activity againt Nalm6 ALL (leukemia) in NSG mice

Project description:SOCS1 is a new intracellular checkpoint abrogating CD4 T cells response with translational value in improving CAR T cells therapies

2021-09-02 | GSE154790 | GEO

Impact of SOCS1 inactivation on OT1 adoptive cell transfer in B16-OVA melanoma C57BL/6 bearing mice

Project description:Role of SOCS1 inactivation on OT1 transferred T cells anti-tumor activity in B16-OVA melanoma tumoirs

2021-09-02 | GSE154792 | GEO

Impact of SOCS1 inactivation on Marilyn adoptive cell transfer in MB49 female C57BL/6 bearing mice

Project description:In vivo, the expansion of antigen experienced CD4+ T cells is limited by intrinsic factors. Using an in vivo genome-wide CRISPR-Cas9 screen, we identified SOCS1 as a major non-redundant checkpoint imposing a brake on antigen experienced CD4+ T-cell proliferation upon antigen challenge. Although SOCS1 has been previously described as an inhibitor of CD8+ T-cell effector function, we highlight here that it is abrogating the CD4+ T-cell response. SOCS1 integrates several cytokines receptor signals to actively silence TCR-induced polycytokine signaling pathways, restraining CD4+ T cell proliferation and functions. Targeting SOCS1 in mouse and human CD4+ and CD8+ T cells improved the therapeutic efficacy of antitumor adoptive T-cell therapies, enhancing intra-tumor T cell accumulation, persistence and effector functions. SOCS1 deletion in CAR-T cells enhances CD4+ CAR T-cell proliferation/survival and polyfunctionality in vivo, promoting long term rejection of established tumors. These findings identify SOCS1 as a major intracellular checkpoint inhibitor of re-stimulated CD4+ T cells, opening new possibilities to optimize adoptive T cell therapies.

2021-09-02 | GSE154791 | GEO

SOCS1

Project description:SOCS1

| PRJNA647451 | ENA

The tumor suppressor SOCS1 diminishes tolerance to oxidative stress in hepatocellular carcinoma

Project description:SOCS1 is a tumor suppressor in hepatocellular carcinoma. Recently we showed that loss of SOCS1 in hepatocytes promotes NRF2 activation. Here we investigated how SOCS1 expression affected oxidative stress response in HCC cells. Murine Hepa1-6 cells expressing SOCS1 (Hepa-SOCS1) or control vector (Hepa-Vector) were treated with cisplatin or tert-butyl hydroperoxide (t-BHP). Induction of NRF2 and its target genes, oxidative stress, lipid peroxidation, cell survival and cellular proteome profiles were evaluated. NRF2 induction was significantly reduced in Hepa-SOCS1 cells. The gene and protein expression of NRF2 targets were differentially induced in Hepa-Vector cells but markedly suppressed in Hepa-SOCS1 cells. Hepa-SOCS1 cells displayed increased induction of reactive oxygen species (ROS) but reduced lipid peroxidation. Nonetheless, Hepa-SOCS1 cells treated with cisplatin or t-BHP showed reduced survival. GCLC, poorly induced in Hepa-SOCS1 cells, showed a strong positive correlation with NFE2L2 and an inverse correlation with SOCS1 in the TCGA-LIHC transcriptomic data. Proteomic analysis of Hepa-Vector and Hepa-SOCS1 cells revealed that SOCS1 differentially modulated many proteins involved in diverse molecular pathways including those implicated in mitochondrial ROS generation and detoxification by peroxiredoxin and thioredoxin systems. Our findings indicate that maintaining sensitivity to oxidative stress is an important tumor suppression mechanism of SOCS1 in HCC.

2024-05-22 | PXD047908 | Pride

RNA-seq on CAR-T cells and CAR-T cells exposed to Nalm6 stimulation followed by treatment with DMSO, BAPTA and BTP-2

Project description:Chimeric antigen receptor (CAR) T cells are known to be potent in recognizing and eliminating tumor elimination, and effector functions. They induce marked responses in patients with refractory leukemia and lymphoma, but dysfunction of T cells is an inevitable obstacle for persistent curative effect. Extending the persistence of these cells without compromising their potency is supposed to improve treatment outcomes. We demonstrated that the SOCE (Store-Operated Calcium Entry) inhibitor BTP-2, rather than calcium chelator BAPTA-AM, diminished exhaustion and terminal differentiation of CAR-T cells both in tonic signaling and tumor antigen exposure models. And BTP-2 pretreated CAR-T cells showed improved antitumor potency and prolonged survival in NSG mice. To further investigate the biological impact of calcium signaling at the molecular level, we performed RNA-seq on CAR-T cells and CAR-T cells exposed to Nalm6 stimulation followed by treatment with DMSO, BAPTA and BTP-2.The high-throughput RNA sequencing (RNA-Seq) revealed that treatment with BTP-2 downregulates glycolysis pathway.

2021-11-19 | GSE178998 | GEO

Treg transcriptomic profile in NSG, NSG+Thymus humanized mice and healthy donors (HD)

Project description:RNA sequencing was performed on RNA extracted from human Treg cells from NSG, NSG+Thymus humanized mice and healthy donors

2021-11-02 | GSE186881 | GEO

PAX5 CHIP-seq in NALM6 cell line

Project description:CHIP-seq performed with no drug treatment in NALM6 cells

2020-01-23 | GSE115764 | GEO

Gene expression profiling in Nalm6 ALL leukemia cells

Project description:Identify the expression intensity for all genes in Nalm6 cells and all the genes are divided into 4 equal groups with group 1 containing the 25% of genes that were expressed at the highest levels, and group 4 containing the 25% of genes that were expressed at the lowest levels. Total RNA are isolated from 3 lots of Nalm6 cells and gene expression are determined by microarray gene expression analysis with Nimblegen Human 385K array.

2015-11-03 | E-GEOD-44214 | biostudies-arrayexpress

SILAC-based quantitative proteomics implicates SOCS1 in modulating protein constituents of large macromolecular complexes in hepatocytes

Project description:Suppressor of Cytokine Signaling 1 (SOCS1) functions as a tumor suppressor in hepatocellular carcinoma by regulating cytokine, growth factor and other signaling pathways. The tumor suppressor functions of SOCS1 are mediated partly via promoting ubiquitination and proteasomal degradation of several signaling proteins. In this study, we used an unbiased approach to characterize SOCS1-mediated changes in the protein profile of hepatocytes. The murine HCC cell line Hepa1-6 transduced with wildtype SOCS1, an SH2 domain mutant or the empty lentiviral vector were grown in Stable Isotopic Labelling of Amino acids in Cell culture (SILAC) media. The cells were stimulated with hepatocyte growth factor or left at steady state. Following cell lysis, proteins were separated on SDS-PAGE gels and peptides extracted by in-gel trypsinization were analyzed by mass spectrometry. Differentially modulated proteins identified and quantified were subjected to pathway enrichment analysis. In total, 3440 proteins were identified in Hepa cells in the presence of SOCS1 at steady state, of which 181 proteins were significantly modulated by SOCS1. The SH2 domain mutation and HGF stimulation increased the number of differentially modulated proteins, which showed only a limited overlap with SOCS1-modulated proteins. Protein interaction network analysis revealed enrichment of SOCS1-modulated proteins within multiprotein complexes such as ubiquitin conjugating enzymes, proteasome, mRNA spliceosome, mRNA exosome and mitochondrial ribosome. Further analysis indicated SOCS1-dependent regulation of the UBE2D ubiquitin conjugating enzymes, which are implicated in growth factor receptor signaling, indirectly via an unknown protein. Given the ubiquitous and highly regulated induction of SOCS1 by diverse cellular stimuli, our findings suggest a fundamental role of SOCS1 in regulating large macromolecular complexes that are important for cellular homeostasis.

2021-02-01 | PXD019135 | Pride

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