ILT3 promotes tumor cell motility and angiogenesis in non-small cell lung cancer

Li, Juan; Gao, Aiqin; Zhang, Fang; Wang, Shuyun; Wang, Jingnan; Wang, Jing; Han, Shuyi; Yang, Zijiang; Chen, Xiaozheng; Fang, Yixuan; Jiang, Guosheng; Sun, Yehuan

doi:10.1016/j.canlet.2020.10.048

Cited by 30 publications

(30 citation statements)

References 36 publications

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“…For example, engagement of ILT3 on myeloid cells by fibronectin resulted in SYK inhibition via SHP1 recruitment, whereas ApoE-ILT3 signals through IKK/ pathway by SHP2 recruitment in leukemia cells but has no effect on non-malignant myeloid cells (20). ILT3 is expressed ectopically on some cancer cells (13,36,37). The ApoE-ILT3 interaction on non-small cell lung cancer cells activates ERK1/2 signaling and results in epithelial-mesenchymal transition and increased vascular endothelial growth factor (VEGF)-A expression (37).…”

Section: Discussionmentioning

confidence: 99%

“…ILT3 is expressed ectopically on some cancer cells (13,36,37). The ApoE-ILT3 interaction on non-small cell lung cancer cells activates ERK1/2 signaling and results in epithelial-mesenchymal transition and increased vascular endothelial growth factor (VEGF)-A expression (37). These diverse responses of ILT3 to its ligands suggest that additional factors are likely involved in a cell-type specific manner to govern the biological outcome of ILT3 engagement.…”

Section: Discussionmentioning

confidence: 99%

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The Fibronectin–ILT3 Interaction Functions as a Stromal Checkpoint that Suppresses Myeloid Cells

Paavola

Roda

Lin

et al. 2021

Cancer Immunology Research

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Y.W. have patent applications on ILT3/Fibronectin blockade. M.C. receives research support from Pfizer and NGM Biopharmaceuticals, is a scientific advisory board member of Vigil Neuroscience and NGM Biopharmaceuticals and consultant of Cell Signaling Technologies. Synopsis:In this study, the fibronectin-ILT3 interaction is shown to represent a "stromal checkpoint" through which the extracellular matrix actively suppresses tumor-associated myeloid cells. Therapeutics targeting this interaction can potentially reprogram suppressive myeloid cells, increasing antitumor immune responses.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The Fibronectin–ILT3 Interaction Functions as a Stromal Checkpoint that Suppresses Myeloid Cells

Paavola

Roda

Lin

et al. 2021

Cancer Immunology Research

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“…Similarly, Li et al. ( 66 ) found that Immunoglobulin-like transcription 3 (ILT3) is enriched in human NSCLC cells, where it activates the SHP2/SHIP1/ERK1/2 axis through interactions with apolipoprotein E (ApoE), thereby inducing VEGF-A expression and promoting tumor angiogenesis. Ubiquitin specific peptidase 22 (USP22) is a ubiquitin-hydrolase that catalytically removes the monoubiquitin portion of histone H2B (H2Bub1).…”

Section: Novel Angiogenic Regulators In Lung Cancer Treatmentmentioning

confidence: 97%

Novel Angiogenic Regulators and Anti-Angiogenesis Drugs Targeting Angiogenesis Signaling Pathways: Perspectives for Targeting Angiogenesis in Lung Cancer

Lin

Wang

et al. 2022

Front. Oncol.

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Lung cancer growth is dependent on angiogenesis. In recent years, angiogenesis inhibitors have attracted more and more attention as potential lung cancer treatments. Current anti-angiogenic drugs targeting VEGF or receptor tyrosine kinases mainly inhibit tumor growth by reducing angiogenesis and blocking the energy supply of lung cancer cells. However, these drugs have limited efficiency, raising concerns about limited scope of action and mechanisms of patient resistance to existing drugs. Therefore, current basic research on angiogenic regulators has focused more on screening carcinogenic/anticancer genes, miRNAs, lncRNAs, proteins and other biomolecules capable of regulating the expression of specific targets in angiogenesis signaling pathways. In addition, new uses for existing drugs and new drug delivery systems have received increasing attention. In our article, we analyze the application status and research hotspots of angiogenesis inhibitors in lung cancer treatment as a reference for subsequent mechanistic research and drug development.

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“…Tumor dissemination and metastasis are primary contributory factors to failure to respond to anticancer therapy and are responsible for 90% of all cancer-related deaths ( 68 , 69 ). Like LILRB2, LILRB4 has been reported to control NSCLC pathogenesis, enhancing widespread NSCLC cell invasion and tumor angiogenesis, and may serve as an alternative strategy for NSCLC treatment ( 69 ). Blockade of LILRB4 expressed on monocytic MDSCs (M-MDSCs) reduces their ability to inhibit T cell responses ( 70 ).…”

Section: Cancermentioning

confidence: 99%

Human inhibitory leukocyte Ig-like receptors: from immunotolerance to immunotherapy

Louche¹,

Roghanian²

2022

JCI Insight

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ILT3 promotes tumor cell motility and angiogenesis in non-small cell lung cancer

Cited by 30 publications

References 36 publications

The Fibronectin–ILT3 Interaction Functions as a Stromal Checkpoint that Suppresses Myeloid Cells

The Fibronectin–ILT3 Interaction Functions as a Stromal Checkpoint that Suppresses Myeloid Cells

Novel Angiogenic Regulators and Anti-Angiogenesis Drugs Targeting Angiogenesis Signaling Pathways: Perspectives for Targeting Angiogenesis in Lung Cancer

Human inhibitory leukocyte Ig-like receptors: from immunotolerance to immunotherapy

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