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POSTN secreted from glioblastoma stem cells can recruit microglia and upregulate CD70 expression in microglia through the αVβ3/PI3K/AKT/NFκB pathway [HMC3_ChIP-seq]

ABSTRACT: Glioblastoma (GBM), classified as a grade 4 glioma, is the most prevalent intrinsic malignancy of the central nervous system. Glioblastoma stem cells (GSCs) are small populations of GBM cells with self-renewal and multilineage differentiation capabilities and are considered responsible for the tumorigenesis and development of GBM. POSTN secreted from glioblastoma stem cells can recruit microglia and upregulate CD70 expression in microglia through the αVβ3/PI3K/AKT/NFκB pathway, which in turn promotes Treg development and functionality and supports the formation of an immunosuppressive tumor microenvironment.

ORGANISM(S): Homo sapiens

PROVIDER: GSE273251 | GEO | 2024/08/01

REPOSITORIES: GEO

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POSTN secreted from glioblastoma stem cells can recruit microglia and upregulate CD70 expression in microglia through the αVβ3/PI3K/AKT/NFκB pathway

Project description:Our findings revealed that POSTN secreted from GSCs can recruit microglia and upregulate CD70 expression in microglia through the αVβ3/PI3K/AKT/NFκB pathway, which in turn promotes Treg development and functionality and supports the formation of an immunosuppressive tumor microenvironment.

2024-08-04 | GSE273464 | GEO

POSTN secreted from glioblastoma stem cells can recruit microglia and upregulate CD70 expression in microglia through the αVβ3/PI3K/AKT/NFκB pathway

Project description:POSTN secreted from glioblastoma stem cells can recruit microglia and upregulate CD70 expression in microglia through the αVβ3/PI3K/AKT/NFκB pathway

| PRJNA1141973 | ENA

POSTN secreted from glioblastoma stem cells can recruit microglia and upregulate CD70 expression in microglia through the αVβ3/PI3K/AKT/NFκB pathway [HMC3_ChIP-seq]

Project description:POSTN secreted from glioblastoma stem cells can recruit microglia and upregulate CD70 expression in microglia through the αVβ3/PI3K/AKT/NFκB pathway [HMC3_ChIP-seq]

| PRJNA1140869 | ENA

POSTN secreted from GSCs promotes GSC self-renewal and tumor growth via activation of the αVβ3/PI3K/AKT/β-catenin/FOSL1 pathway [GSCs_CHIP-seq]

Project description:Glioblastoma (GBM), classified as a grade 4 glioma, is the most prevalent intrinsic malignancy of the central nervous system. Glioblastoma stem cells (GSCs) are small populations of GBM cells with self-renewal and multilineage differentiation capabilities and are considered responsible for the tumorigenesis and development of GBM. GSCs also exhibit radiation resistance, chemoresistance, and angiogenic and invasive properties, which are correlated with poor outcomes in GBM patients. Therefore, targeting GSCs constitutes a promising approach for treating GBM patients. Our findings revealed that POSTN secreted from GSCs promotes GSC self-renewal and tumor growth via activation of the αVβ3/PI3K/AKT/β-catenin/FOSL1 pathway.

2024-08-01 | GSE273250 | GEO

POSTN secreted from GSCs promotes GSC self-renewal and tumor growth via activation of the αVβ3/PI3K/AKT/β-catenin/FOSL1 pathway [GSCs_RNA-seq]

2024-08-01 | GSE273252 | GEO

CD70 as an actionable immunotherapeutic target in recurrent glioblastoma and its microenvironment

Project description:We have used our established Glioblastoma cell models and gene expression analyses to characterize gene wild-type and CD70 knockdown GBM cell lines

2022-09-01 | GSE182295 | GEO

Analysis of CD70 wild type or CD70 knock out CD70-specific nanoCAR T cells

Project description:CD70 is an attractive target for chimeric antigen receptor (CAR) T cell therapy as treatment for both solid and liquid malignancies. However, functionality of CD70-specific CAR T cells is only modest. Here, we optimized a CD70-specific VHH based CAR (nanoCAR). We evaluated the nanoCARs in clinically relevant models in vitro, using co-cultures of CD70-specific nanoCAR T cells with malignant rhabdoid tumor organoids, and in vivo by using a diffuse large B cell lymphoma (DLBCL) patient-derived xenograft (PDX) model. Whereas the nanoCAR T cells were highly efficient in organoid co-cultures, they showed only modest efficacy in the PDX model. Knocking out CD70 expression in the nanoCAR T cells resulted in dramatically enhanced functionality in the PDX model, suggesting that CD70 interaction in cis with the nanoCAR induces exhaustion. Through single-cell transcriptomics, we obtained evidence that CD70 KO CD70-specific nanoCAR T cells are protected from antigen-induced exhaustion. Our data show that CARs targeted to endogenous T cell antigens, negatively affect CAR T cell functionality by inducing an exhausted state, which can be overcome by knocking out the specific target, in this case CD70.

2024-06-17 | GSE227435 | GEO

Analysis of CD70 wild type or CD70 knock out CD70-specific nanoCAR T cells [RNA-Seq]

Project description:CD70 is an attractive target for chimeric antigen receptor (CAR) T-cell therapy for the treatment of both solid and liquid malignancies. However, the functionality of CD70-specific CAR T-cells is modest. We optimized a CD70-specific VHH-based CAR (nanoCAR). We evaluated the nanoCARs in clinically relevant models in vitro, using co-cultures of CD70-specific nanoCAR T-cells with malignant rhabdoid tumor organoids, and in vivo using a diffuse large B-cell lymphoma (DLBCL) patient-derived xenograft (PDX) model. Whereas the nanoCAR T-cells were highly efficient in organoid co-cultures, they showed only modest efficacy in the PDX model. Fratricide was not causing this loss in efficacy but rather CD70 interaction in cis with the nanoCAR, as validated by imaging flowcytometry, induces exhaustion. Knocking out CD70 expression in nanoCAR T-cells using CRISPR/Cas9, resulted in dramatically enhanced functionality in the DLBCL PDX model. Through single-cell transcriptomics, we obtained evidence that CD70 knock out (KO) CD70-specific nanoCAR T-cells were protected from antigen-induced exhaustion. In addition, we were able to demonstrate that WT CD70-specific nanoCAR T-cells already exhibit signs of exhaustion shortly after production. Their gene signature strongly overlapped with gene signatures of exhausted CAR T-cells. On the other hand, the gene signature of KO nanoCAR T-cells overlapped with the gene signature of CAR T-cell infusion products that led to complete responses in chronic lymphatic leukemia patients. Our data show that CARs targeting endogenous T-cell antigens, negatively affect CAR T-cell functionality by inducing an exhausted state, which can be overcome by knocking out the specific target, in this case CD70.

2024-06-17 | GSE265937 | GEO

Novel Thyrointegrin αvβ3 antagonist (fp-PMT) with potent affinity in the treatment of cancer

Project description:Microarray analysis was carried out on Glioblastoma (GBM 10181360, GBM 021913 and U87 cells), Bladder cancer (JBV253), skin cancer (A375) and Acute Myelod Leukemia (AML) (KG1A and K562 cells) exposed to fb-PMT at 30 µM concentration. Our genome-wide microarray screens demonstrated that fb-PMT appears to exert its potent anticancer actions on human cancer cells through the molecular interference mechanism with multiple signaling pathways supporting growth and survival of leukemic cells. Notably, fb-PMT had a significant effect on different molecular pathways that contribute to the anticancer activity such as cell cycle control (MYC), survival and maintenance of stem cells (HIF1A; TFAP2C), essential features of the malignant phenotype (TWIST1; SNAI). Furthermore, the fb-PMT-induced significant transcriptional pathway’s activation includes RB1; IRF9; MAML1; RAP1A; and GATA4 pathways, which known to play an important role in anticancer activity. Finally, Consistent with our previous reports on the crosstalk between integrin αvβ3 and ERα which contributes to the induced proliferation of cancer cells, we found that fb-PMT interference with estrogen signaling. The αvβ3 agonist (thyroid hormone) was associated with increased phosphorylation and nuclear enrichment of estrogen receptor α (ERα).

2021-09-11 | GSE183772 | GEO

Microglia polarization and anti-glioma effects fostered by dual cell membrane-coated doxorubicin-loaded hexagonal boron nitride nanoplatelets

Project description:Glioblastoma multiforme (GBM) is a highly malignant brain cancer, and microglial cells play a critical role in its progression. Activation of microglia can either promote or inhibit GBM growth depending on the stage of tumour development and on the microenvironment. As current treatments for GBM have limited efficacy, there is an urgent need to develop novel strategies based on nanoplatforms for drug delivery and efficient targeting. This study investigated the microglial response and the therapeutic efficacy of dual cell membrane-coated and doxorubicin-loaded hexagonal boron nitride nanoplatelets, tested on human microglia and GBM cells. The results showed promising therapeutic effects on glioma cells and an M2 microglia polarization, highlighted through proteomic analysis.

2024-01-26 | PXD043557 | Pride

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