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RNA sequencing analysis for mouse ovarian cancer cells and tumors response to B7-H3 (Cd276) depletion

ABSTRACT: RNA sequencing analysis for mouse ovarian cancer cells and tumors response to B7-H3 (Cd276) depletion

PROVIDER: PRJNA728566 | ENA |

REPOSITORIES: ENA

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RNA sequencing analysis for mouse ovarian cancer cells and tumors response to B7-H3 (Cd276) depletion

Project description:Analysis of mouse ovarian cancer cell lines HM-1 and ID8, and HM-1 tumors inoculated to B6C3F1 mice with B7-H3 (Cd276) knockout (KO) by CRISPR-Cas9. We identified B7-H3 expression is upregulated in IFN-γ–low, PD-L1–low non-immunoreactive tumors of high grade serous ovarian cancer. We explored the influence of B7-H3 on immune evasion outside of its direct regulatory function on target cells by generating B7-H3 knockout cell lines and tumors in syngeneic mouse models.

2022-01-10 | GSE174137 | GEO

mTORC1 upregulates B7-H3/CD276 to inhibit antitumor T cells and drive tumor immune evasion [CITE-Seq]

Project description:Immune checkpoints are often expressed on tumor cells; it remains a prevailing need to identify the mechanisms underlying their regulation and therapeutic benefit. The immune checkpoint molecule B7-H3 is upregulated in many human tumors, including those with high mechanistic/mammalian target of rapamycin complex (mTORC1) activity. However, its role in tumor immunity and the impact of B7-H3-targeted therapy on the tumor immune microenvironment are largely uncharacterized. Here, we used a syngeneic murine model of tuberous sclerosis complex (TSC), a model of mTORC1 hyperactivity, to assess the mechanisms by which B7-H3 remodels the tumor microenvironment. We performed gene and protein expression profiling analysis using data generated from CITE-seq of infiltrating CD3+ T cells isolated by FACS from subcutaneous B7-H3 knockdown and control TSC2-deficient 105K tumors.

2023-02-08 | GSE213939 | GEO

mTORC1 upregulates B7-H3/CD276 to inhibit antitumor T cells and drive tumor immune evasion [RNA-seq]

Project description:Immune checkpoints are often expressed on tumor cells; it remains a prevailing need to identify the mechanisms underlying their regulation and therapeutic benefit. The immune checkpoint molecule B7-H3 is upregulated in many human tumors, including those with high mechanistic/mammalian target of rapamycin complex (mTORC1) activity. Still, its role in tumor immunity and the impact of B7-H3-targeted therapy on the tumor immune microenvironment are largely uncharacterized in mTORC1-hyperactive tumors. Here, we used a syngeneic murine model of tuberous sclerosis complex (TSC), a model of mTORC1 hyperactivity, to assess the mechanisms by which B7-H3 remodels the tumor microenvironment. We performed gene expression profiling analysis using data generated from RNA-seq of bulk tumors from subcutaneous B7-H3 knockdown and control TSC2-deficient 105K cells or sorted tumor cells isolated by MACS mouse tumor cell isolation kit (Miltenyi Biotec).

2023-02-08 | GSE213626 | GEO

Targeting Osteosarcoma with Canine B7-H3 CAR T Cells and Impact of CXCR2 Co-Expression on Functional Activity

Project description:Abstract. The use of large animal spontaneous models of solid cancers, such as dogs with osteosarcoma (OS), can help develop new cancer immunotherapy approaches, including chimeric antigen receptor (CAR) T cells. Therefore, the goal of the present study was to generate canine CAR T cells targeting the B7-H3 (CD276) co-stimulatory molecule overexpressed by several solid cancers, including OS and glioma in both humans and dogs, and to assess their ability to recognize B7-H3 expressed by canine OS cell lines or by canine tumors in xenograft models. A second objective was to determine whether a novel dual CAR that expressed a chemokine receptor together with the B7-H3 CAR improved the activity of the canine CAR T cells. Therefore, in the studies reported here we examined B7-H3 expression by canine OS tumors, evaluated target engagement by canine B7-H3 CAR T cells in vitro, and compared the relative effectiveness of B7-H3 CAR T cells versus B7-H3-CXCR2 dual CAR T cells in canine xenograft models. We found that most canine OS tumors expressed high levels of B7-H3, whereas levels were undetectable on normal dog tissues. In vitro, both B7-H3 CAR T cells demonstrated activation and OS-specific target killing in vitro, but there was significantly greater cytokine production by B7-H3-CXCR2 CAR T cells. In canine OS xenograft models, little antitumor activity was generated by B7-H3 CAR T cells, whereas B7-H3-CXCR2 CAR T cells significantly inhibited tumor growth, inducing complete tumor elimination in most treated mice. These findings indicated therefore that addition of a chemokine receptor could significantly improve the anti-tumor activity of canine B7-H3 CAR T cells, and that evaluation of this new dual CAR construct in dogs with primary or metastatic OS is warranted since such studies could provide a critical and realistic validation of the chemokine receptor concept.

2024-04-03 | GSE247355 | GEO

MiR-1253 exerts tumor-suppressive effects in medulloblastoma via inhibition of CDK6 and CD276 (B7-H3)

Project description:MiR-1253 exerts tumor-suppressive effects in medulloblastoma via inhibition of CDK6 and CD276 (B7-H3)

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CD276 is an important player in macrophage recruitment into the tumor and an upstream regulator for PAI-1

Project description:70-100% of colorectal, prostate, ovarian, pancreatic and breast cancer specimens show expression of CD276 (B7-H3), a potential immune checkpoint family member. Several studies have shown that high CD276 expression in cancer cells correlates with a poor clinical prognosis. This has been associated with the presence of lower tumor infiltrating leukocytes. Among those, tumor-associated macrophages can comprise up to 50% of the tumor mass and are thought to support tumor growth through various mechanisms. However, a lack of information on CD276 function and interaction partner(s) impedes rigorous evaluation of CD276 as a therapeutic target in oncology. Therefore, we aimed to understand the relevance of CD276 in tumor-macrophage interaction by employing a 3D spheroid coculture system with human cells. Our data show a role for tumor-expressed CD276 on the macrophage recruitment into the tumor spheroid, and also in regulation of the extracellular matrix modulator PAI-1. Furthermore, our experiments focusing on macrophage-expressed CD276 suggest that the antibody-dependent CD276 engagement triggers predominantly inhibitory signaling networks in human macrophages.

2021-07-28 | GSE165610 | GEO

RNA sequencing comparison of B7-H3.TMIGD2 and B7-H3.CD28.4-1BB CAR-T cells in vitro

Project description:CAR-T cell costimualtory domains can alter CAR-T cell phenotypes. We therefore performed RNA sequencing to understand the effect of TMIGD2 vs CD28.4-1BB comstimulation in B7-H3 CAR-T cells after in vitro coculture.

2024-05-08 | GSE254544 | GEO

Rh-30 micro array data, knockdown of PAX3-FOXO1 and B7-H3

Project description:To investigate the effect of PAX3-FOXO1 and B7-H3 in rhabdomyosarcoma, Rh-30 (PAX3-FOXO1 positive rhabdomyosarcoma cell line) was transfected by siPAX3-FOXO1 or siB7-H3. After knockdown, total RNA was extracted and analyzed. As a result, some genes and pathways, such as chemotaxis, differentiation, and INF-gamma production were comonnly effected by PAX3-FOXO1 and B7-H3.

2019-03-02 | GSE127703 | GEO

RNA sequencing comparison of B7-H3.TMIGD2 and B7-H3.CD28.4-1BB CAR-T cells in vivo.

Project description:The tumor microenvironment can significantly alter CAR-T cell phenotypes. We therefore performed RNA sequencing to understand the effect of TMIGD2 vs CD28.4-1BB comstimulation in B7-H3 CAR-T cells after intravenous administration to tumor-bearing mice in vivo.

2024-05-08 | GSE254545 | GEO