ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024
CD147-K148me2-Driven Tumor Cell-Macrophage Crosstalk Provokes NSCLC Immunosuppression via the CCL5/CCR5 Axis.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed.
- Bispecific ANXA2/CD147 CAR-T cell therapy for osteosarcoma.Oncogene · 2026Article
- Protein modification systems as cancer biomarkers and therapeutic targets.Precision clinical medicine · 2026Review
- TCGA-Informed Spatial Profiling Reveals Peripheral CD147 Expression at the Invasive Tumor Front as a Prognostic Indicator in OSCC.International journal of molecular sciences · 2026Article
- Employing epigenetic protein degradation techniques to block CCL5-mediated photodynamic therapy via a programmed delivery platform.Signal transduction and targeted therapy · 2026Article
- SAMHD1 drives immunosuppression in non-small cell lung cancer by promoting macrophage infiltration and restricting oncolytic adenovirus replication.Journal for immunotherapy of cancer · 2026Article
- Mechanisms of transcriptional regulation of CCR5, which is the co-receptor for R5-tropic HIV and is also involved in other disease processes.Biochemical Society transactions · 2026Review
- From description to prediction: a multi-database bibliometric forecast-validation study of lung cancer and tumor-associated macrophages research (2005-2025).Frontiers in immunology · 2026Review
- Nanoparticles that modulate immune cells - an important strategy for the future treatment of tumors.Frontiers in immunology · 2026Review
- Review
- Unraveling the molecular-pathological characteristics and cellular complexity of the tumor immune microenvironment in metastatic non-small cell lung cancer.Cell communication and signaling : CCS · 2025Review
- Scaffolding Protein ENH Promotes Tumor Angiogenesis and Growth Through Macrophage Recruitment and Polarization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- A multifunctional biomimetic nanoplatform combined with immune checkpoint blockade for triple-negative breast cancer immunotherapy through inhibiting polarization of M2 macrophages.Journal of nanobiotechnology · 2025Article
- NSD proteins in anti-tumor immunity and their therapeutic targeting by protein degraders.Cellular and molecular life sciences : CMLS · 2025Review
- Tumor-infiltrating lymphocytes in NSCLC: from immune surveillance to immunotherapy.Frontiers in immunology · 2025Review
- CD147-K148me2-Driven Tumor Cell-Macrophage Crosstalk Provokes NSCLC Immunosuppression via the CCL5/CCR5 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- CD8Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
19 authors.
Funding
Abstract
Immunosuppression is a major hallmark of tumor progression in non-small cell lung cancer (NSCLC). Cluster of differentiation 147 (CD147), an important pro-tumorigenic factor, is closely linked to NSCLC immunosuppression. However, the role of CD147 di-methylation in the immunosuppressive tumor microenvironment (TME) remains unclear. Here, di-methylation of CD147 at Lys148 (CD147-K148me2) is identified as a common post-translational modification (PTM) in NSCLC that is significantly associated with unsatisfying survival outcomes among NSCLC sufferers, especially those in the advanced stages of the disease. The methyltransferase NSD2 catalyzes CD147 to generate CD147-K148me2. Further analysis demonstrates that CD147-K148me2 reestablishes the immunosuppressive TME and promotes NSCLC progression. Mechanistically, this modification promotes the interaction between cyclophilin A (CyPA) and CD147, and in turn, increases CCL5 gene transcription by activating p38-ZBTB32 signaling, leading to increased NSCLC cell-derived CCL5 secretion. Subsequently, CD147-K148me2-mediated CCL5 upregulation facilitates M2-like tumor-associated macrophage (TAM) infiltration in NSCLC tissues via CCL5/CCR5 axis-dependent intercellular crosstalk between tumor cells and macrophages, which is inhibited by blocking CD147-K148me2 with the targeted antibody 12C8. Overall, this study reveals the role of CD147-K148me2-driven intercellular crosstalk in the development of NSCLC immunosuppression, and provides a potential interventional strategy for PTM-targeted NSCLC therapy.
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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.