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Tumor cell-intrinsic BTLA receptor inhibits the proliferation of tumor cells via ERK1/2

ABSTRACT: Tumor cell-intrinsic BTLA receptor inhibits the proliferation of tumor cells via ERK1/2

PROVIDER: PRJNA855884 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19978276_1.fastq.gz	Fastqsanger.gz
	SRR19978276_2.fastq.gz	Fastqsanger.gz
	SRR19978277_1.fastq.gz	Fastqsanger.gz
	SRR19978277_2.fastq.gz	Fastqsanger.gz
	SRR19978278_1.fastq.gz	Fastqsanger.gz

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Tumor cell-intrinsic BTLA receptor inhibits the proliferation of tumor cells via ERK1/2

Project description:B and T lymphocyte attenuator (BTLA) is an immune checkpoint molecule that mediates the escape of tumor cells from immunosurveillance. Consequently, BTLA and its ligand-herpesvirus entry mediator （HVEM） are potentially immunotherapeutic targets. However, the potential effects of BTLA on tumor cells remain incompletely unknown. Here, we show that BTLA is expressed across a broad range of tumor cells. The depletion of BTLA or HVEM promotes cell proliferation and colony formation，which is reversed by re-overexpression of BTLA in BTLA knockout (KO) cells. On the contrary, overexpression of BTLA or HVEM inhibits tumor cell proliferation and colony formation. Furthermore, the proliferation of subpopulation with high BTLA is also significantly slower than that of the low BTLA subpopulation. Mechanistically, the coordination of BTLA and HVEM inhibits its major downstream ERK1/2 signaling pathway, thus preventing tumor cell growth. This study demonstrates that tumor cell-intrinsic BTLA/HVEM is a potential tumor suppressor and likely to have potential antagonist for immunotherapy, thus representing a potential biomarker for the optimal cancer immunotherapeutic treatment.

2022-12-12 | GSE207471 | GEO

Expression data from FACS-sorted CD8+BTLA+ vs CD8+BTLA- Human Tumor-infiltrating Lymphocytes in Metastatic Melanoma

Project description:Adoptive T-cell Therapy (ACT) involves using tumor-infiltrating lymphocytes (TIL) isolated from metastatic melanoma and expanding them ex vivo prior to infusion into lympho-depleted patients. This is one of the most promising approaches to treat metastatic melanoma, with the rates of clinical response between 48-50% based on studies done at NCI, M.D. Anderson Cancer Center (Houston, TX), and Sheba Medical Center (Tel Aviv, Israel). In the Phase II ACT Trial at M.D. Anderson Cancer Center , our group has uncovered an association between positive clinical response and the amount of CD8+ tumor-infiltrating lymphocytes expressing B and T Lymphocyte Attenuator (BTLA), a reported inhibitory receptor on T-cells. We used microarrays to detail the differences in the global programme of gene expression between CD8+BTLA+ vs CD8+BTLA- TILs in order to understand the molecular basis of the clinical association. TILs were isolated by enzymatically digest the melanoma tumor fragments obtained from Stage IIIc/IV melanoma patients at M.D. Anderson Cancer Center. The TILs were expanded with high-dose IL-2 for two weeks prior to sorting by FACS (fluoresecence-activated cell sorter) for CD8+BTLA+ and CD8+BTLA- susbets. RNA was extracted from each sorted subsets and hybridized on Affymetrix microarrays

2013-01-03 | E-GEOD-43260 | biostudies-arrayexpress

Tumor Cell-Intrinsic BTLA Receptor Inhibits the Proliferation of Tumor Cells via ERK1/2.

Project description:B and T lymphocyte attenuator (BTLA) is an immune checkpoint molecule that mediates the escape of tumor cells from immunosurveillance. Consequently, BTLA and its ligand herpesvirus entry mediator (HVEM) are potentially immunotherapeutic targets. However, the potential effects of BTLA on tumor cells remain incompletely unknown. Here, we show that BTLA is expressed across a broad range of tumor cells. The depletion of BTLA or HVEM promotes cell proliferation and colony formation, which is reversed by the overexpression of BTLA in BTLA knockout cells. In contrast, overexpression of BTLA or HVEM inhibits tumor cell proliferation and colony formation. Furthermore, the proliferation of a subpopulation with high BTLA was also significantly slower than that of the low BTLA subpopulation. Mechanistically, the coordination of BTLA and HVEM inhibits its major downstream extracellular regulated protein kinase (ERK1/2) signaling pathway, thus preventing tumor cell growth. This study demonstrates that tumor cell-intrinsic BTLA/HVEM is a potential tumor suppressor and is likely to have a potential antagonist for immunotherapy, thus representing a potential biomarker for the optimal cancer immunotherapeutic treatment.

| S-EPMC9777428 | biostudies-literature

Expression data from FACS-sorted CD8+BTLA+ vs CD8+BTLA- Human Tumor-infiltrating Lymphocytes in Metastatic Melanoma

2013-01-03 | GSE43260 | GEO

BTLA NTN scRNAseq

Project description:BTLA NTN scRNAseq

| PRJNA926654 | ENA

BTLA interacting proteins in mouse CD4+ effector T cells - Part2

Project description:Identifying BTLA interacting proteins in mouse CD4+ effector T cells expressing BTLA at endogenous levels and after stimulation with pervanadate.

2019-05-06 | PXD010863 | Pride

BTLA NTN scRNAseq

Project description:Goal is to investigate the molecular changes in renal leukocytes during nephrotoxic nephritis in BTLA-KO mice compared to wild-type mice

2023-07-22 | GSE223534 | GEO

Thymocytes TCR repertoire from regular B6 and Btla KO mice

Project description:Deletion of BTLA up regulates CD5 expression. Higher CD5 expression during thymic selection is associated with increased self-recognition, suggesting that BTLA might be needed early to establish self-tolerance. To investigate whether the regulation of CD5 by BTLA is TCR-repertoire independent, we performed single-cell TCR sequencing in SP CD4 thymocytes from regular B6 and B6 Btla Knock-Out (KO) mice.

2024-11-06 | GSE269212 | GEO

Analysis of BTLA regulated transcripts in human B and CD4+ T cells

Project description:Purified B or CD4+ T cells were analyzed for transcriptional changes induced by the BTLA inhibitory receptor. BTLA receptors were activated using anti-human BTLA coupled to microbeads. Gene expression was analyzed using Nanostring

2022-01-28 | GSE194314 | GEO

BTLA and PD-1 signals attenuate TCR-mediated gene expression

Project description:T cell coinhibitory immune checkpoints, such as PD-1 or BTLA, are bona fide targets in cancer therapy. Here we used a human T cell reporter line to measure transcriptome changes mediated by PD-1 and BTLA induced signalling. TCR/CD3 stimulation resulted in the upregulation of a large number of genes but also repressed a similar number of transcripts. PD-1 and BTLA signals attenuated transcriptomics changes mediated by TCR/CD3 signalling: upregulated genes tended to be suppressed and the expression of a significant number of downregulated genes was higher when PD-1 or BTLA signalling took place. BTLA was a significantly stronger attenuator of TCR/CD3 induced transcriptome changes than PD-1. A strong overlap between genes that were regulated indicated quantitative rather than qualitative differences between these receptors. In line with their function as attenuator of TCR/CD3 mediated changes we found strongly regulated genes to be prime targets of PD-1 and BTLA signalling.

2024-05-27 | GSE239586 | GEO

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