ArticleJournal of immunology research2020
Preferential Expression of B7-H6 in Glioma Stem-Like Cells Enhances Tumor Cell Proliferation via the c-Myc/RNMT Axis.
Article in Journal of immunology research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- Defining substrate specificities of human RNA capping methyltransferases through quantitative assessment of independent yet cooperative activities.Protein science : a publication of the Protein Society · 2026Article
- Association between elevated serum soluble B7-H6 and infection in hemodialysis patients.Clinical and experimental nephrology · 2025Article
- RNMT-dependent RNA cap methylation in health and disease.The Biochemical journal · 2025Review
- Sohlh1 Modulates the Stemness and Differentiation of Glioma Stem-Like Cells by Inactivation of Wnt/β-Catenin Signalling Pathway via SFRP1.Journal of cellular and molecular medicine · 2025Article
- Characterisation of RNA guanine-7 methyltransferase (RNMT) using a small molecule approach.The Biochemical journal · 2025Article
- Immune checkpoints in immune response to glioma: two sides of the same coin.Frontiers in immunology · 2025Review
- The role of RNA methylation in glioma progression: mechanisms, diagnostic implications, and therapeutic value.Frontiers in immunology · 2025Review
- Harnessing B7-H6 for Anticancer Immunotherapy: Expression, Pathways, and Therapeutic Strategies.International journal of molecular sciences · 2024Review
- The role of RNA methylation in tumor immunity and its potential in immunotherapy.Molecular cancer · 2024Review
- Kinetic characterization of human mRNA guanine-N7 methyltransferase.Scientific reports · 2024Article
- Insights into the regulatory role of RNA methylation modifications in glioma.Journal of translational medicine · 2023Review
- Review
- Deficiency of N-linked glycosylation impairs immune function of B7-H6.Frontiers in immunology · 2023Article
- N7-methylguanosine modification: from regulatory roles to therapeutic implications in cancer.American journal of cancer research · 2023Review
- Construction and Validation of a Novel Prognostic Signature of Idiopathic Pulmonary Fibrosis by Identifying Subtypes Based on Genes Related to 7-Methylguanosine Modification.Frontiers in genetics · 2022Article
- The immunosuppressive microenvironment and immunotherapy in human glioblastoma.Frontiers in immunology · 2022Review
- Role of B7 family members in glioma: Promising new targets for tumor immunotherapy.Frontiers in oncology · 2022Review
- B7-H6 is a new potential biomarker and therapeutic target of T-lymphoblastic lymphoma.Annals of translational medicine · 2021Article
- Interaction network of immune-associated genes affecting the prognosis of patients with glioblastoma.Experimental and therapeutic medicine · 2021Article
- All-trans retinoic acid induces leukemia resistance to NK cell cytotoxicity by down-regulating B7-H6 expression via c-Myc signaling.Cancer communications (London, England) · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
B7 homologue 6 (B7-H6), a newly identified member of the B7 costimulatory molecule family, is not only a crucial regulator of NK cell-mediated immune responses through binding to NKp30 but also has clinical implications due to its abnormal expression in human cancers. Here, we show that B7-H6 expression is abnormally upregulated in glioma tissue and that B7-H6 is coexpressed with stem cell marker Sox2. Intriguingly, B7-H6 was rarely detected on the surface of glioma cell lines but was abundantly expressed in glioma stem-like cells (GSLCs) that were derived from the glioma cell lines
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.