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Human CD26high T cells elicit tumor immunity against multiple malignancies via enhanced migration and persistence

ABSTRACT: Human CD26high T cells elicit tumor immunity against multiple malignancies via enhanced migration and persistence

PROVIDER: PRJNA417933 | ENA |

REPOSITORIES: ENA

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Human CD26high T cells elicit tumor immunity against multiple malignancies via enhanced migration and persistence

Project description:CD8+ T lymphocytes mediate potent immune responses against tumor, but the role of human CD4+ T cell subsets in cancer immunotherapy remains ill-defined. Herein, we exhibit that CD26 identifies three T helper subsets with distinct immunological properties in both healthy individuals and cancer patients. Although CD26neg T cells possess a regulatory phenotype, CD26int T cells are mainly naive and CD26high T cells appear terminally differentiated and exhausted. Paradoxically, CD26high T cells persist in and regress multiple solid tumors following adoptive cell transfer. Further analysis revealed that CD26high cells have a rich chemokine receptor profile (including CCR2 and CCR5), profound cytotoxicity (Granzyme B and CD107A), resistance to apoptosis (c-KIT and Bcl2), and enhanced stemness (β-catenin and Lef1). These properties license CD26high T cells with a natural capacity to traffic to, regress and survive in solid tumors. Collectively, these findings identify CD4+ T cell subsets with properties critical for improving cancer immunotherapy

2017-11-11 | GSE106726 | GEO

Human CD26high T cells elicit tumor immunity against multiple malignancies via enhanced migration and persistence.

Project description:CD8+ T lymphocytes mediate potent immune responses against tumor, but the role of human CD4+ T cell subsets in cancer immunotherapy remains ill-defined. Herein, we exhibit that CD26 identifies three T helper subsets with distinct immunological properties in both healthy individuals and cancer patients. Although CD26neg T cells possess a regulatory phenotype, CD26int T cells are mainly naive and CD26high T cells appear terminally differentiated and exhausted. Paradoxically, CD26high T cells persist in and regress multiple solid tumors following adoptive cell transfer. Further analysis revealed that CD26high cells have a rich chemokine receptor profile (including CCR2 and CCR5), profound cytotoxicity (Granzyme B and CD107A), resistance to apoptosis (c-KIT and Bcl2), and enhanced stemness (?-catenin and Lef1). These properties license CD26high T cells with a natural capacity to traffic to, regress and survive in solid tumors. Collectively, these findings identify CD4+ T cell subsets with properties critical for improving cancer immunotherapy.

| S-EPMC5719008 | biostudies-literature

Quassinoid analogs with enhanced efficacy for treatment of hematologic malignancies specifically target the PI3Kgamma isoform

Project description:Development of novel PI3Ks inhibitors is an important strategy to overcome their resistance and poor tolerability in clinical trials. The quassinoid family member Brusatol shows specific inhibitory activity against hematologic malignancies. However, the mechanism of its anti-cancer activity is unknown. We studied the anti-cancer activity of Brusatol on multiple hematologic malignancies derived cell lines by RNA-Seq, mass spectrometry, biochemical pull-down assays, and CRISPR/Cas9 gene knock-out. We demonstrated that the PI3Kgamma isoform was identified as a direct target of Brusatol, and inhibition was lost on PI3Kgamma deficient cells. Novel synthetic analogs were also developed and tested in vitro and in vivo. They shared superior potency in their ability to inhibit malignant hematologic cell lines, and in a xenograft transplant mouse model. They also had minimal toxicity to normal human cells. These new analogs have enhanced potential for development as a new class of PI3K inhibitors for treatment of hematologic malignancies.

2020-03-06 | MSV000085067 | MassIVE

Inactivating Negative Regulators of Cortical Branched Actin Enhances Persistence of Single Cell Migration.

Project description:Inactivating Negative Regulators of Cortical Branched Actin Enhances Persistence of Single Cell Migration.

| PRJNA1026159 | ENA

Listeria Persistence

Project description:Listeria Persistence

| PRJEB1356 | ENA

Listeria Persistence

Project description:Listeria Persistence

| PRJEB1355 | ENA

Overexpression of histone demethylase Fbxl10 leads to enhanced migration in mouse embryonic fibroblasts

Project description:Cell migration is a central process in the development and maintenance of multicellular organisms. Tissue formation during embryonic development, wound healing, immune responses and invasive tumors all require the orchestrated movement of cells to specific locations. Histone demethylase proteins alter transcription by regulating the chromatin state at specific gene loci. FBXL10 is a conserved and ubiquitously expressed member of the JmjC domain-containing histone demethylase family and is implicated in the demethylation of H3K4me3 and H3K36me2 and thereby removing active chromatin marks. However, the physiological role of FBXL10 in vivo remains largely unknown. Therefore, we established an inducible gain of function model to analyze the role of Fbxl10 and compared wild-type with Fbxl10 overexpressing mouse embryonic fibroblasts (MEFs). Our study shows that overexpression of Fbxl10 in MEFs doesn`t influence the proliferation capability but leads to an enhanced migration capacity in comparison to wild-type MEFs. Transcriptome and ChIP-seq experiments demonstrated that Fbxl10 binds to genes involved in migration like Areg, Mdk, Lmnb1, Thbs1, Mgp and Cxcl12. Taken together, our results strongly suggest that Fbxl10 plays a critical role in migration by binding to the promoter region of migration-associated genes and thereby might influences cell behaviour to a possibly more aggressive phenotype.

2016-10-01 | GSE86090 | GEO

Early Onset Malignancies Initiative

Project description:Early Onset Malignancies Initiative

| PRJNA597501 | ENA

Early Onset Malignancies Initiative

Project description:Early Onset Malignancies Initiative

| PRJNA597502 | ENA

Inactivating Negative Regulators of Cortical Branched Actin Enhances Persistence of Single Cell Migration.

Project description:Here we show that enhancing polymerization of branched actin at the cell cortex by removing as many as 3 negative regulators promotes single cell migration, but not collective migration of mammary epithelial cells

2023-10-14 | GSE244924 | GEO

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