B7-H3 as a Novel CAR-T Therapeutic Target for Glioblastoma

Tang, Xin; Zhao, Shasha; Zhang, Yang; Wang, Yuelong; Zhang, Zongliang; Yang, Meng; Zhu, Yan‐Yu; Zhang, Guanjie; Guo, Gang; Tong, Aiping; Zhou, Liangxue

doi:10.1016/j.omto.2019.07.002

Cited by 155 publications

(103 citation statements)

References 32 publications

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“…Antitumor effects of B7-H3-specific CAR-T cells were also assessed in primary glioblastoma cell lines. The specific antitumor functions of CAR-T cells were confirmed both in vitro and in vivo [57]. There is rapid development of antibody drugs and CAR-T cells that target B7-H3, which may be administered alone or may achieve synergistic anti-tumor effects when combined with chemotherapeutic agents or other therapeutic regimens.…”

Section: Targeting B7-h3 Therapymentioning

confidence: 86%

B7-H3, a checkpoint molecule, as a target for cancer immunotherapy

2020

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B7-H3 (also known as CD276) is a newly found molecule of B7 family, which may be a promising target for cancer treatment. B7-H3 protein was demonstrated to be expressed in several kinds of tumor tissues including non-small-cell lung cancer (NSCLC) and prostate cancer. Its expression is highly associated with undesirable treatment outcomes and survival time, due to function of the immune checkpoint molecule. It was classified as either a co-stimulatory molecule for T cell activation or the nonimmunological role of regulating signaling pathways. Although there is still no agreed conclusion on the function of B7-H3, it may be a valuable target for cancer therapy. This review aims to provide a comprehensive, up-to-date summary of the advances in B7-H3 targeting approaches in cancer therapy. Although several challenges remain, B7-H3 offers a new therapeutic target with increased efficacy and less toxicity in future cancer treatment.

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Section: Targeting B7-h3 Therapymentioning

confidence: 86%

B7-H3, a checkpoint molecule, as a target for cancer immunotherapy

2020

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“…To elucidate the possible mechanism by which lncRNA SLC8A1-AS1 regulates the proliferation, clone formation, migration and invasion of glioma cell, Western-blot analysis of the key molecular factors of cancer-related pathways, such as Hippo pathway, Wnt/β-catenin pathway was performed. The Wnt/βcatenin pathway plays a key role in tumor EMT [17][18][19]. GSK-3β is one of the components of the destruction complex in the Wnt/β-catenin signaling [20].…”

Section: Discussionmentioning

confidence: 99%

Knockdown long noncoding RNA SLC8A1-AS1 attenuate cell invasion and migration in glioma via suppression of Wnt-β catenin signaling pathways

Yang

Zhu

Zhang

et al. 2020

Preprint

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Background Glioma, as the most common aggressive malignant tumor in the central nervous system, is still an insurmountable disease in neural system. The potential mechanism of its carcinogenesis remains largely unclear. Methods In the present study, we identified dysregulated lncRNA solute carrier family 8 member A1 antisense RNA 1 (SLC8A1-AS1) as associated with glioma based on The Cancer Genome Atlas (TCGA)data. Validation experiment was conducted to confirm a high expression level of lncRNA SLC8A1-AS1 in glioma tissues. Results Down-regulation of lncRNA SLC8A1-AS1 suppressed proliferation, clone formation, migration and invasion of glioma cells in vitro and in vivo. Moreover, lncRNA SLC8A1-AS1 silencing decreased the activity of the Wnt/β-catenin pathway and suppressed the epithelial to mesenchymal transition (EMT) in glioma cells. Conclusions Collectively, these findings provide a novel insights into the function and mechanism of lncRNA SLC8A1-AS1 in the pathogenesis of glioma and highlight its potential as a therapeutic target for glioma intervention.

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“…Trivalent CAR T cells targeting three glioblastoma associated antigens (HER2, IL-13Rα2-, and EphA2-specific CAR molecules, all expressed simultaneously on the T cell surface) are now designed [94]. Even more recently, other antigens have been targeted including CSPG4 [95] or B7-H3 [96] and chlorotoxin [97] as has been eloquently demonstrated in preclinical studies. These proof-of-concept studies are promising; however, the question remains if these CAR T cell products will be efficient when tested clinically [91].…”

Section: Strategies To Enhance the Efficacy Of Adoptive Transfer Of Ementioning

confidence: 99%

Immunotherapy in Glioblastoma: Current Shortcomings and Future Perspectives

Weenink

French

Smitt

et al. 2020

Cancers

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Glioblastomas are aggressive, fast-growing primary brain tumors. After standard-of-care treatment with radiation in combination with temozolomide, the overall prognosis of newly diagnosed patients remains poor, with a 2-year survival rate of less than 20%. The remarkable survival benefit gained with immunotherapy in several extracranial tumor types spurred a variety of experimental intervention studies in glioblastoma patients. These ranged from immune checkpoint inhibition to vaccinations and adoptive T cell therapies. Unfortunately, almost all clinical outcomes were universally disappointing. In this perspective, we provide an overview of immune interventions performed to date in glioblastoma patients and re-evaluate their performance. We argue that shortcomings of current immune therapies in glioblastoma are related to three major determinants of resistance, namely: low immunogenicity; immune privilege of the central nervous system; and immunosuppressive micro-environment. In this perspective, we propose strategies that are guided by exact shortcomings to sensitize glioblastoma prior to treatment with therapies that enhance numbers and/or activation state of CD8 T cells.

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B7-H3 as a Novel CAR-T Therapeutic Target for Glioblastoma

Cited by 155 publications

References 32 publications

B7-H3, a checkpoint molecule, as a target for cancer immunotherapy

B7-H3, a checkpoint molecule, as a target for cancer immunotherapy

Knockdown long noncoding RNA SLC8A1-AS1 attenuate cell invasion and migration in glioma via suppression of Wnt-β catenin signaling pathways

Immunotherapy in Glioblastoma: Current Shortcomings and Future Perspectives

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