Tumor-expressed B7-H3 promotes vasculogenic mimicry formation rather than angiogenesis in non-small cell lung cancer

Fan, Xingyu; Huang, Junfeng; Hu, Bingqi; Zhou, Jing; Chen, Liwen

doi:10.1007/s00432-023-04790-3

Cited by 3 publications

(2 citation statements)

References 52 publications

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“…B7-H3 also promotes lung cancer EMT as suggested by its correlation with the mesenchymal marker n-cadherin and vimentin [ 50 ]. Vasculogenic mimicry, which is an alternative microvascular circulation independent of angiogenesis, is promoted B7-H3 expressing NSCLC tumor cell that act via PI3K/AKT signaling pathway [ 177 ]. Furthermore, B7-H3 orchestrates SCLC metabolic reprogramming as it enhances glucose uptake, extracellular acidification rate, and oxygen consumption rate, while its deletion significantly decreases the activation of several oncogenic signaling pathways, including ERK, AKT, and STAT3 [ 178 ].…”

Section: Lung Cancermentioning

confidence: 99%

New Emerging Targets in Cancer Immunotherapy: The Role of B7-H3

Koumprentziotis,

Theocharopoulos,

Foteinou

et al. 2024

Vaccines

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Immune checkpoints (ICs) are molecules implicated in the fine-tuning of immune response via co-inhibitory or co-stimulatory signals, and serve to secure minimized host damage. Targeting ICs with various therapeutic modalities, including checkpoint inhibitors/monoclonal antibodies (mAbs), antibody-drug conjugates (ADCs), and CAR-T cells has produced remarkable results, especially in immunogenic tumors, setting a paradigm shift in cancer therapeutics through the incorporation of these IC-targeted treatments. However, the large proportion of subjects who experience primary or secondary resistance to available IC-targeted options necessitates further advancements that render immunotherapy beneficial for a larger patient pool with longer duration of response. B7-H3 (B7 Homolog 3 Protein, CD276) is a member of the B7 family of IC proteins that exerts pleiotropic immunomodulatory effects both in physiologic and pathologic contexts. Mounting evidence has demonstrated an aberrant expression of B7-H3 in various solid malignancies, including tumors less sensitive to current immunotherapeutic options, and has associated its expression with advanced disease, worse patient survival and impaired response to IC-based regimens. Anti-B7-H3 agents, including novel mAbs, bispecific antibodies, ADCs, CAR-T cells, and radioimmunotherapy agents, have exhibited encouraging antitumor activity in preclinical models and have recently entered clinical testing for several cancer types. In the present review, we concisely present the functional implications of B7-H3 and discuss the latest evidence regarding its prognostic significance and therapeutic potential in solid malignancies, with emphasis on anti-B7-H3 modalities that are currently evaluated in clinical trial settings. Better understanding of B7-H3 intricate interactions in the tumor microenvironment will expand the oncological utility of anti-B7-H3 agents and further shape their role in cancer therapeutics.

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Section: Lung Cancermentioning

confidence: 99%

New Emerging Targets in Cancer Immunotherapy: The Role of B7-H3

Koumprentziotis,

Theocharopoulos,

Foteinou

et al. 2024

Vaccines

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“…VM is an alternative microcirculation pattern independent of angiogenesis, where cancer cells form microvascular-like channels to provide nutrients and oxygen to tumors ( 59 ). Recent studies have found that B7-H3 expressed in tumors promotes VM formation in non-small cell lung cancer cells through the PI3K/AKT signaling pathway without affecting normal angiogenesis, providing a new strategy for future anticancer therapies ( 42 ). The summary of signaling pathways mediating B7-H3-induced tumor angiogenesis is presented in Table 1 .…”

Section: The Role Of B7-h3 In Tumor Vasculature and Clinical Treatmentmentioning

confidence: 99%

Non-immune functions of B7-H3: bridging tumor cells and the tumor vasculature

Wu,

Hu,

Hui

et al. 2024

Front. Oncol.

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B7-H3 (CD276), an immune checkpoint molecule, is overexpressed in various types of cancer and their tumor vasculature, demonstrating significant associations with adverse clinical outcomes. In addition to its well-known immune functions, B7-H3 exhibits dual co-stimulatory/co-inhibitory roles in normal physiology and the tumor microenvironment. The non-immune functions of B7-H3 in tumor cells and the tumor vasculature, including promoting tumor cell anti-apoptosis, proliferation, invasion, migration, drug resistance, radioresistance, as well as affecting cellular metabolism and angiogenesis, have increasingly gained attention from researchers. Particularly, the co-expression of B7-H3 in both tumor cells and tumor endothelial cells highlights the higher potential and clinical utility of therapeutic strategies targeting B7-H3. This review aims to summarize the recent advances in understanding the non-immune functions of B7-H3 in tumors and provide insights into therapeutic approaches targeting B7-H3, focusing on its co-expression in tumor cells and endothelial cells. The aim is to establish a theoretical foundation and practical reference for the development and optimization of B7-H3-targeted therapies.

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