CD47
- Known as:
- CD47
- Catalog number:
- 1F-225-T100
- Product Quantity:
- 100 tests
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD47
Related genes to: CD47
- Gene:
- CD47 NIH gene
- Name:
- CD47 molecule
- Previous symbol:
- MER6
- Synonyms:
- IAP, OA3
- Chromosome:
- 3q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-12
- Date modifiied:
- 2016-10-05
Related products to: CD47
Related articles to: CD47
- CD47 is an innate immune checkpoint that can protect tumor cells from macrophage-mediated clearance, but the regulatory mechanisms underlying its expression in ovarian cancer (OC) remain incompletely understood. Here, we investigated the epigenetic regulation of CD47 expression in OC. Single-cell and spatial transcriptomic analyses indicated preferential CD47 expression in malignant epithelial cells. Integration of publicly available epigenomic datasets revealed a distal regulatory region with enhancer-associated features across ovarian cancer models and HGSOC patient samples. A genome-wide CRISPR-Cas9 screen further implicated PITX2 and EP300 as regulators of CD47 expression. Chromatin immunoprecipitation assay showed PITX2 and EP300 occupancy at candidate enhancer elements within this CD47 regulatory region. Comparative epigenomic analyses suggested that features of this regulatory landscape are also present in fallopian tube epithelial cells and become more prominent in OC. suTogether, these findings support a PITX2-EP300 regulatory axis associated with CD47 expression and provide evidence for its potential contribution to tumor immune evasion. - Source: PubMed
Publication date: 2026/09/10
Mishra Alok KBiswas TanayRoy AnjanBanday ShahidKatiyar ArpitSharma AnshulLi RuiZhu Lihua JulieMalonia Sunil KAteeq Bushra - CD47 is a major innate immune checkpoint molecule that interacts with signal regulatory protein α (SIRPα) to deliver a "don't eat me" signal and restrain macrophage-mediated phagocytosis. Accumulating evidence indicates that dysregulated CD47 expression is associated with immune escape, treatment resistance, and adverse clinicopathological features in several digestive system cancers, although the strength of these associations varies across tumor types. This narrative review provides an integrative overview of CD47 structure, ligand interactions, signaling and immune-regulatory functions, and summarizes reported expression patterns and available evidence regarding regulatory mechanisms and relevant mechanistic contexts in esophageal, gastric, colorectal, hepatocellular, pancreatic, and biliary tract cancers. We further review therapeutic strategies targeting the CD47-SIRPα axis, including anti-CD47 antibodies, SIRPα fusion proteins, bispecific antibodies, and emerging cell-based and nanotechnology-based platforms, with particular attention to recent clinical developments. Finally, we critically discuss translational challenges, including hematologic toxicity and antigen sink, assay standardization and biomarker selection, resistance mechanisms, optimization of combination regimens, and the need for prospective validation of hypothesis-generating biomarker signals. By integrating recent 2025-2026 clinical developments with mechanistic and engineering advances, including lessons from unsuccessful or discontinued clinical programs, this review provides a balanced perspective on the opportunities and remaining barriers to the clinical translation of CD47-directed therapy in digestive system cancers. - Source: PubMed
Publication date: 2026/09/03
Sun HaolinWei ChenyuLong JianglanLiu XiaojiaLi QuanfuCao Bangwei - This study aimed to evaluate CD47 expression in nonsmall-cell lung cancer (NSCLC) and explore the predictive value of combined CD47 and programmed death-ligand 1 (PD-L1) status for immunotherapy outcomes. - Source: PubMed
Publication date: 2026/09/29
Miao ShengchaoGuan YapingChen HuananCheng YuxiaLiu HongtaoGuo YanYe Xin - Triple-negative breast cancer (TNBC) is an aggressive subtype lacking effective targeted therapies. A multitarget gene therapy was developed and validated to overcome molecular heterogeneity and compensatory survival signaling in TNBC. A codon-optimized human transcriptional intermediary factor 1 gamma (opti-hTIF1γ) gene therapy was evaluated in ex vivo-cultured patient biopsy tissues and in orthotopic and mammary intraductal mouse models, and the underlying mechanisms were investigated using pathway and immune-functional analyses. Ex vivo findings were further validated using patient-derived cells and complementary mechanistic studies, including ubiquitination assays, chromatin immunoprecipitation, and functional macrophage coculture analyses, to define the molecular basis of TIF1γ-mediated antitumor activity. Transduction of opti-hTIF1γ to ex vivo-cultured biopsy tissues from TNBC patients suppressed epithelial-to-mesenchymal transition and proliferation while inducing apoptosis. In orthotopic and mammary intraductal mouse models, opti-hTIF1γ effectively suppressed tumor growth and lung metastasis. Mechanistically, opti-hTIF1γ inhibits β-catenin via ubiquitination-dependent degradation and inhibits the SMAD-dependent TGFβ pathway by binding to SMAD2/3. In parallel, it suppresses the SMAD-independent TGFβ pathway via ubiquitination and caspase-3-associated degradation of STAT3, leading to the inhibition of TAK1. Furthermore, opti-hTIF1γ downregulates STAT3-dependent immune modulators such as CD47 and CXCL5 in TNBC, enhancing macrophage phagocytosis. These findings position opti-hTIF1γ as a promising multitarget gene therapeutic strategy for TNBC through concurrent suppression of tumorigenic signaling and reprogramming of the immune landscape. - Source: PubMed
Publication date: 2026/09/29
Park HyominKim Tae YoonYun HyunjiCha AreumMoon DodamYun EugeneKim YoungminIm Seock-AhLee Dae-WonPark ChangheeKim Hong-KyuLee Han-ByoelLee JaewonCho Nam-JoonLee Eun JuKim Hyo-Soo - The transmembrane protein CD47 expressed on tumor cells suppresses Fcγ receptor-mediated antibody-dependent cellular phagocytosis (ADCP) through its interaction with signal regulatory protein α (SIRPα), a transmembrane protein expressed on phagocytic cells such as macrophages. Although blockade of the CD47-SIRPα interaction enhances the efficacy of tumor-targeting antibodies such as rituximab, its antitumor activity remains limited in cancers lacking defined tumor-associated antigens. In this study, we identified the membrane protein Basigin and SIRPα as broadly applicable therapeutic targets for cancer. We found that the 8H4 antibody, originally identified in the course of other research, recognized mouse Basigin, suppressed proliferation of diverse cancer cell types, and induced cancer cell death. Treatment with the 8H4 antibody indeed inhibited tumor growth in vivo. Moreover, combined treatment with the 8H4 antibody and an anti-SIRPα antibody that blocks the CD47-SIRPα interaction markedly enhanced macrophage-mediated ADCP against diverse cancer cell types in vitro. These results suggest that targeting Basigin, particularly in combination with SIRPα blockade, may provide a basis for the development of macrophage-mediated immunotherapies applicable to cancers in which tumor-associated antigens have not yet been identified. - Source: PubMed
Publication date: 2026/08/31
Yang YiyanTakai TomokoHatano NaoyaMurata YojiMatozaki TakashiManiwa YoshimasaKotani Takenori