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STIM1 and STIM2 mediate cancer-induced inflammation in T cell acute lymphoblastic leukemia

ABSTRACT: STIM1 and STIM2 mediate cancer-induced inflammation in T cell acute lymphoblastic leukemia

PROVIDER: PRJNA480224 | ENA |

REPOSITORIES: ENA

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STIM1 and STIM2 mediate cancer-induced inflammation in T cell acute lymphoblastic leukemia

Project description:T-cell acute lymphoblastic leukemia (T-ALL) is a malignancy of T cell progenitors that in most patients is associated with activating mutations in the NOTCH1 pathway. Recent reports have indicated a link between Ca2+ homeostasis in the endoplasmic reticulum (ER), the regulation of NOTCH1 signaling and T-ALL. Here we investigated the role of store-operated Ca2+ entry (SOCE) in T-ALL. SOCE is a Ca2+ influx pathway that is mediated by the plasma membrane Ca2+ channel ORAI1 and its activators STIM1 and STIM2. Deletion of STIM1 and STIM2 in leukemic cells abolished SOCE and significantly prolonged the survival of mice in a NOTCH1-driven model of T-ALL. The survival advantage was unrelated to leukemia development and leukemic cell burden, but was associated with the SOCE-dependent ability of malignant T lymphoblasts to cause inflammation in leukemia-infiltrated organs. Mice with wildtype T-ALL showed a severe necroinflammatory response in their bone marrow, which was absent in mice with Stim1/2-/- leukemia. Several signaling pathways previously linked to cancer-induced inflammation were downregulated in Stim1/2-/- leukemic cells, likely accounting for less aggressive leukemia progression and prolonged survival of mice. Our study shows that T-ALL is associated with inflammation of leukemia-infiltrated organs and that SOCE controls the proinflammatory effects of leukemic T lymphoblasts.

2018-07-11 | GSE116776 | GEO

STIM1 and STIM2 Mediate Cancer-Induced Inflammation in T Cell Acute Lymphoblastic Leukemia.

Project description: Not available

| S-EPMC6170166 | biostudies-literature

Proteogenomics of High hyperdiploid childhood acute lymphoblastic leukemia

Project description:Proteogenomic analysis and genomic profiling, RNA-sequencing, and mass spectrometry-based analysis of High hyperdiploid childhood acute lymphoblastic leukemia.

2019-02-25 | PXD010175 | Pride

STIM1 controls T cell mediated immune regulation and inflammation in chronic infection

Project description:Influence of STIM1 on the transcriptome of CD4+ T cell subsets STIM1 is critical for the regulation of the intracellular Ca2+ homeostasis in CD4+ T cell. Loss of function mutations in STIM1 in patients result in severe immuno deficiency and recurrent infections. Using conditional knock out mice for STIM1, we investigated the role of STIM1 in T cells during chronic infections by in-vivo and in-vitro experiments. We found that STIM1 is required for T cell-mediated immunity to chronic infection with Mycobacterium tuberculosis (Mtb) as STIM1-deficient mice succumb to infection faster than littermate controls, have increased mycobacterial burdens and severe pulmonary infiltration with myeloid and lymphoid cells .Using the Affymetrix Mouse Exon 1.0 platform, we analyzed the influence of STIM1 expression on the transcriptom of CD4+T cells in-vitro. We found that STIM1 is required for the regulation of apoptosis related genes after TCR stimulation as well as for the induction of a transcriptonal program that polarizes naive CD4+ T cells into inducible CD4+ T regulatory cells (iTreg). Together with our in-vivo findings, these experiments reveal that STIM1 is essential for immune regulation to prevent an injurious inflammatory response during chronic infection.

2015-03-17 | GSE66933 | GEO

Proteogenomics of High hyperdiploid childhood acute lymphoblastic leukemia

Project description:Proteogenomic analysis and genomic profiling, RNA-sequencing, and mass spectrometry-based analysis of High hyperdiploid childhood acute lymphoblastic leukemia.

2020-01-29 | MSV000084862 | MassIVE

Metabolomics of B-cell Acute Lymphoblastic Leukemia in Response to Adipocyte Conditioned Media

Project description:Adipocyte conditioned media (ACM), stromal cell conditioned media (SCM) and unconditioned media (UCM) were added to B-cell Acute Lymphoblastic Leukemia cells (REH and RCH-AcV) either with or without methotrexate (MTX). The metabolomic profiles of the cells was determined by mass spectrometry.

2022-10-07 | ST002383 | MetabolomicsWorkbench

MicroRNA-sequencing of Brazilian pediatric acute lymphoblastic leukemia

Project description:MicroRNA-sequencing of the bone marrow samples from Brazilian pediatric patients with B-cell acute lymphoblastic leukemia (B-ALL) and T-cell acute lymphoblastic leukemia (T-ALL).

2022-04-13 | E-MTAB-11621 | biostudies-arrayexpress

STIM1 Translocation to The Nucleus Protects Cells from DNA Damage

Project description:DNA damage represents a challenge for cells as this damage must be eliminated to preserve cell viability and the transmission of genetic information. To reduce or eliminate unscheduled chemical modifications in genomic DNA, an extensive signaling network, known as the DNA damage response (DDR) pathway, ensures this repair. In this work, and by means of a proteomic analysis aimed at the study of the STIM1 protein interactome, we have found that STIM1 is closely related to the protection from endogenous DNA damage, replicative stress, as well as in the response to interstrand crosslinks (ICLs). Here we show that STIM1 has a nuclear localization signal (NLS) that mediates its translocation to the nucleus, and that this translocation and the association of STIM1 to chromatin is enhanced in response to mitomycin C (MMC), an ICL-inducing agent. Consequently, STIM1-deficient cell lines show a higher level of basal DNA damage, replicative stress, and a higher sensitivity to MMC. We show that STIM1 normalizes FANCD2 protein levels in the nucleus, explaining the increased sensitivity to MMC in STIM1-KO cells. Our results show for the first time a nuclear function for the endoplasmic reticulum protein STIM1 and increase the number of genes involved in DNA repair.

2023-12-22 | PXD041181 | Pride

Expression profile of select glucose and lipid metabolic genes mediated by STIM1 knockout, or STIM1 knockout plus Snail1 overexpression in SMMC7721 cells

Project description:To investigate the altered glucose and lipid metabolism genes after STIM1 knockout (STIM1 KO) or STIM1 knockout plus Snail1 OE (STIM1 KO+Snail1 OE) in SMMC7721 cells. STIM1 KO-SMMC7721 cells were constructed by CRISPR/Cas9, and STIM1 KO+Snail1 OE-SMMC7721 cells was established via lentiviral Infection of Snail1 overexpression in STIM1 KO-SMMC7721 cells. The cells mentioned above were cultured in DMEM supplemented with 10% (v/v) FBS at 37 °C in 5% CO2. When the cells grow to 60~70% confluent, total RNA was extracted by using Trizol (TAKARA, Japan). Reverse transcription was performed from 1μg total RNA using PrimeScript™ RT reagent Kit with gDNA Eraser (TAKARA), Quantitative real-time PCR were performed (CFX386, BioRad) with 40 cycles at 95 °C for 10 seconds, 59 °C for 20 seconds and 72 °C for 30 seconds.

2020-04-07 | GSE148129 | GEO

Transcription profiling of human T-cell acute lymphoblastic leukemia, T-cell lymphoblastic lymphoma and B-precursor acute lymphoblastic leukemia samples

Project description:T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoblastic lymphoma (T-LL) and are often thought to represent a spectrum of a single disease. The malignant cells in T-ALL and T-LL are morphologically indistinguishable, and they share the expression of common cell surface antigens and cytogenetic characteristics. However, despite these similarities, differences in the predominant sites of disease in T-ALL and T-LL are observed. To determine if underlying biological distinctions may potentially contribute to some of these differences, we analyzed the global gene expression profiles of malignant T-cell precursors in ten T-ALL and nine T-LL using DNA arrays. Ten additional B-precursor ALL bone marrow samples, were used in a separate analysis. <br><br> Note that files GSM27087.txt and GSM27088.txt are identical as downloaded from GEO.

2007-08-13 | E-GEOD-1577 | biostudies-arrayexpress

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