4
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      The prognostic value of B7-H6 in esophageal squamous cell carcinoma

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          B7-H6, a member of the B7 family molecules, participates in the clearance of tumor cells by binding to NKp30 on NK cells. B7-H6 expression level in esophageal squamous cell carcinoma (ESCC) and the clinical value remain unknown. The goal of this study was to determine the expression of B7-H6 in ESCC and further explore its clinical significance. We retrospectively collected the clinical data of 145 patients diagnosed with ESCC between January 2007 and December 2008. The expression of B7-H6 of the pathological tissue samples was detected by immunohistochemistry. The chi-square (χ 2) test was used to analyse the relationships of B7-H6 and clinicopathological characteristics. Survival and hazard functions were estimated using the Kaplan-Meier method, and survival between groups was compared using the two-sided log-rank test. The Cox proportional hazards regression model was used to adjust for the risk factors related to overall survival (OS). 133/145 (91.72%) of the ESCC tissue samples exhibited B7-H6 expression. The expression level of B7-H6 was correlated with T stage ( P = 0.036) and lymphatic metastasis status ( P = 0.044). High B7-H6 expression ( P = 0.003) was associated with a significantly worse OS than low B7-H6 expression. Multivariate Cox proportional hazards regression analysis demonstrated that tumour size ( P = 0.021), B7-H6 expression ( P = 0.025) and lymphatic metastasis status ( P = 0.049) were independent prognostic factors of OS for ESCC. Collectively, our findings suggest that B7-H6 is widely expressed in ESCC samples. And B7-H6 may represent a predictor of poor prognosis for ESCC.

          Related collections

          Most cited references29

          • Record: found
          • Abstract: found
          • Article: found
          Is Open Access

          The B7 family member B7-H6 is a tumor cell ligand for the activating natural killer cell receptor NKp30 in humans

          Cancer development is often associated with the lack of specific and efficient recognition of tumor cells by the immune system. Natural killer (NK) cells are lymphocytes of the innate immune system that participate in the elimination of tumors. We report the identification of a tumor cell surface molecule that binds NKp30, a human receptor which triggers antitumor NK cell cytotoxicity and cytokine secretion. This previously unannotated gene belongs to the B7 family and, hence, was designated B7-H6. B7-H6 triggers NKp30-mediated activation of human NK cells. B7-H6 was not detected in normal human tissues but was expressed on human tumor cells, emphasizing that the expression of stress-induced self-molecules associated with cell transformation serves as a mode of cell recognition in innate immunity.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            New B7 Family Checkpoints in Human Cancers.

            T cells are the main effector cells in immune response against tumors. The activation of T cells is regulated by the innate immune system through positive and negative costimulatory molecules. Targeting immune checkpoint regulators such as programmed cell death 1 (PD-1)/PD-1 ligand 1 (PD-L1) and CTL antigen 4 (CTLA-4) has achieved notable benefit in a variety of cancers, which leads to multiple clinical trials with antibodies targeting the other related B7/CD28 family members. Recently, five new B7 family ligands, B7-H3, B7-H4, B7-H5, B7-H6, and B7-H7, were identified. Here we review recent understanding of new B7 family checkpoint molecules as they have come to the front of cancer research with the concept that tumor cells exploit them to escape immune surveillance. The aim of this article is to address the structure and expression of the new B7 family molecules as well as their roles in controlling and suppressing immune responses of T cells as well as NK cells. We also discuss clinical significance and contribution of these checkpoint expressions in human cancers. Mol Cancer Ther; 16(7); 1203-11. ©2017 AACR.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Human leukocyte antigen-B-associated transcript 3 is released from tumor cells and engages the NKp30 receptor on natural killer cells.

              The activity of natural killer (NK) cells is regulated by surface receptors, which direct target cell recognition. NKp30 (Natural Cytotoxicity Receptor 3) induces target cell lysis and is also crucial for the interaction with dendritic cells. So far, the cellular ligands for NKp30 have remained elusive. Here we show that the nuclear factor HLA-B-associated transcript 3 (BAT3) was released from tumor cells, bound directly to NKp30, and engaged NKp30 on NK cells. BAT3 triggered NKp30-mediated cytotoxicity and was necessary for tumor rejection in a multiple myeloma model. These data identify BAT3 as a cellular ligand for NKp30. We propose a concept for target cell recognition by NK cells beyond "missing self" and "induced self," mediated through a tumor cell-derived extracellular factor.
                Bookmark

                Author and article information

                Contributors
                caixy@sysucc.org.cn
                y665925@126.com
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                2 December 2019
                2 December 2019
                2019
                : 9
                : 18122
                Affiliations
                [1 ]ISNI 0000 0004 1758 4014, GRID grid.477976.c, Department of Oncology, , The First Affiliated Hospital of Guangdong Pharmaceutical University, ; Guangzhou, Guangdong China
                [2 ]ISNI 0000 0004 1803 6191, GRID grid.488530.2, Department of VIP Region, , Sun Yat-Sen University Cancer Center, ; Guangzhou, Guangdong China
                [3 ]ISNI 0000 0000 8877 7471, GRID grid.284723.8, Department of Radiotherapy, , Huiyang Hospital Affiliated Southern Medical University, ; Huizhou, Guangdong China
                Article
                54731
                10.1038/s41598-019-54731-9
                6889130
                31792298
                a9a9aebd-18fb-45cc-aaba-3d77a60a549c
                © The Author(s) 2019

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 12 July 2019
                : 18 November 2019
                Categories
                Article
                Custom metadata
                © The Author(s) 2019

                Uncategorized
                oesophageal cancer,tumour biomarkers
                Uncategorized
                oesophageal cancer, tumour biomarkers

                Comments

                Comment on this article