Ontology highlight
ABSTRACT:
PROVIDER: PRJEB16971 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Ectothiorhodospira magna B7-7 genome sequencing
| PRJNA329726 | ENA
Project description:B7-H4 functions as an immune checkpoint in the tumor microenvironment (TME). However, the post-translational modification (PTM) of B7-H4 and its translational potential in cancer remains incompletely understood. We found that ZDHHC3, a zinc finger DHHC-type palmitoyltransferase, palmitoylates B7-H4 at Cys130 in breast cancer cells, preventing its lysosomal degradation and sustaining B7-H4-mediated immunosuppression. Knockdown of ZDHHC3 in tumors resulted in robust anti-tumor immunity and reduced tumor progression in murine models. Moreover, abemaciclib, a CDK4/6 inhibitor, primed lysosome activation and promoted lysosomal degradation of B7-H4 independently of the tumor cell cycle. Treatment with abemaciclib resulted in T cell activation and mitigated B7-H4-mediated immune suppression via inducing B7-H4 degradation in preclinical tumor models. Thus, B7-H4 palmitoylation is an undocumented PTM controlling B7-H4 protein stability and abemaciclib may be repurposed to enhance B7-H4 degradation, thereby treating patients with B7-H4+ tumors.
2025-02-14 | PXD054393 | Pride
Project description:This SuperSeries is composed of the following subset Series: GSE29854: Daphnia magna exposed to narcotics and polar narcotics - aniline GSE29856: Daphnia magna exposed to narcotics and polar narcotics - 4-chloroaniline GSE29857: Daphnia magna exposed to narcotics and polar narcotics - 3,5-dichloroaniline GSE29858: Daphnia magna exposed to narcotics and polar narcotics - 2,3,4-trichloroaniline GSE29862: Daphnia magna exposed to narcotics and polar narcotics - ethanol GSE29864: Daphnia magna exposed to narcotics and polar narcotics - isopropanol GSE29867: Daphnia magna exposed to narcotics and polar narcotics - methanol Refer to individual Series
2012-02-01 | E-GEOD-29993 | biostudies-arrayexpress
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
Project description:B7-H3 (CD276), part of the B7 superfamily, has been shown to play an immunomodulatory role, however its regulation, receptor, and mechanism of action remain unclear. Protein levels of B7-H3 have been previously shown to relate to prostate cancer outcomes and currently, humanized monoclonal antibodies are being investigated for clinical therapeutic use (enoblituzumab, MGA271, Macrogenics). Here we use genomic expression data to examine the relationship of B7-H3 to prostate cancer clinical characteristics and molecular profile.
2016-05-12 | GSE79956 | GEO
Project description:Ectothiorhodospira shaposhnikovii overview
| PRJNA37163 | ENA
Project description:Ectothiorhodospira mobilis overview
| PRJNA808128 | ENA
Project description:Ectothiorhodospira variabilis overview
| PRJNA808144 | ENA
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
Project description:B7-H3, an immune checkpoint molecule, is overexpressed in various solid cancers, correlating with negative prognosis and poor clinical outcomes. However, its regulatory mechanisms in aggressive cancers and cancer stem cells (CSCs), which contribute to cancer formation, progression, chemoresistance, and recurrence, remain unclear. To elucidate the mechanisms regulating B7-H3 expression in breast CSCs, we employed DNA affinity purification-mass spectrometry (DAP-MS) with presumptive promoter regions of B7-H3 and identified several proteins binding to that promoter regions in CSC specific manner. Subsequent validation studies identified several potential transcription factors, including DNA damage-binding protein 1 (DDB1), XRCC5, PARP1, RPA1, and RPA3, for their significant impact on B7-H3 expression. In vitro inhibition of DDB1 with its known inhibitor, nitazoxanide, resulted in a marked decrease in B7-H3 expression, suppressing tumor sphere formation and cell migration in breast CSCs. Our findings reveal a transcription factor-mediated regulatory mechanism for B7-H3 in CSCs through proteomic analysis and highlight the critical role of these transcription factors in regulating B7-H3 expression. These results may elucidate underlying mechanisms, paving the way for the development of new immunotherapeutic strategies against breast cancer.
2025-05-07 | PXD054584 | Pride