ArticleOncotarget2015
Immunoglobulin-like transcript 4 promotes tumor progression and metastasis and up-regulates VEGF-C expression via ERK signaling pathway in non-small cell lung cancer.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 43 citations in OpenAlex.
- LILRB2 inhibition by blocking antibody ES009 reprograms immunosuppressive myeloid cells and enhances T-cell-mediated tumor immunity.Human vaccines & immunotherapeutics · 2026Article
- Review
- Targeting leukocyte immunoglobulin‑like receptor B2 in the tumor microenvironment: A new treatment prospect for solid tumors (Review).Oncology letters · 2025Review
- Nanomaterial-Driven Regulated Cell Death: Mechanistic Insights and Novel Strategies for Tumor Therapy.International journal of nanomedicine · 2025Review
- Targeting ILT4 to Improve Immunotherapy Efficacy in Solid Tumour: From Bench to Bedside.ImmunoTargets and therapy · 2025Review
- Inhibitory leukocyte immunoglobulin-like receptors, subfamily B (LILRBs) in human diseases: structure, roles, mechanisms, and clinical applications.Theranostics · 2025Review
- ILT4 facilitates angiogenesis in non-small cell lung cancer.Cancer science · 2024Article
- Dexamethasone promotes renal fibrosis by upregulating ILT4 expression in myeloid-derived suppressor cells.Journal of cellular and molecular medicine · 2024Article
- Strategies for Overcoming Immune Evasion in Bladder Cancer.International journal of molecular sciences · 2024Review
- Analysis of HLA-G 14 bp Insertion/Deletion Polymorphism and HLA-G, ILT2 and ILT4 Expression in Head and Neck Squamous Cell Carcinoma Patients.Diseases (Basel, Switzerland) · 2024Article
- Leukocyte immunoglobulin-like receptor B2 overexpression as a promising therapeutic target and noninvasive screening biomarker for colorectal cancer.World journal of gastroenterology · 2023Article
- Comprehensive analysis of LILR family genes expression and tumour-infiltrating immune cells in early-stage pancreatic ductal adenocarcinoma.IET systems biology · 2023Article
- HLA and tumour immunology: immune escape, immunotherapy and immune-related adverse events.Journal of cancer research and clinical oncology · 2023Review
- Tumor-derived Immunoglobulin-like transcript 4 facilitates angiogenesis of colorectal cancer.American journal of cancer research · 2023Article
- Analysis of the expression and prognosis for leukocyte immunoglobulin-like receptor subfamily B in human liver cancer.World journal of surgical oncology · 2022Article
- Tumor-derived ILT4 induces T cell senescence and suppresses tumor immunity.Journal for immunotherapy of cancer · 2021Article
- Prognostic Significance of Immune Checkpoints HLA-G/ILT-2/4 and PD-L1 in Colorectal Cancer.Frontiers in immunology · 2021Article
- ILT4 in Colorectal Cancer Cells Induces Suppressive T Cell Contexture and Disease Progression.OncoTargets and therapy · 2021Article
- ILT4 inhibition prevents TAM- and dysfunctional T cell-mediated immunosuppression and enhances the efficacy of anti-PD-L1 therapy in NSCLC with EGFR activation.Theranostics · 2021Article
- The Molecular and Functional Characteristics of HLA-G and the Interaction with Its Receptors: Where to Intervene for Cancer Immunotherapy?International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immunoglobulin-like transcript (ILT) 4 has long been thought to be cell-surface molecule in certain immune cells and negatively regulates immune response. Recently, overexpression of ILT4 has been observed in a few cancers with unknown function. Here, we showed manipulation of ILT4 affected non-small cell lung cancer (NSCLC) cell proliferation, migration and invasion in vitro analyses. In vivo, ILT4 promoted the tumor growth and metastasis. Furthermore, the phosphorylation of extracellular regulated protein kinases (ERK1/2) was enhanced in ILT4 overexpressing NSCLC cells. ERK1/2 specific inhibitor U0126 suppressed the proliferation, migration and invasion of those cells. Stepwise investigations demonstrated that vascular endothelial growth factor C (VEGF-C) was the downstream effector of ILT4 and ERK1/2. Silence of VEGF-C attenuated the migration and invasion activity of ILT4 overexpressing cells. Moreover, Kaplan-Meier survival analysis indicated that NSCLC patients with ILT4 positive expression had a poor patient survival. ILT4 and VEGF-C expression had notable positive correlation in cancer cells, and their co-expression was significantly associated with adverse prognostic factors. Our findings suggest that ILT4 drives NSCLC development in part on activation of ERK signaling which in turn upregulates VEGF-C. ILT4 could be a novel cancer therapeutic target for NSCLC.
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