ArticleCancer immunology, immunotherapy : CII2012
SCF and TLR4 ligand cooperate to augment the tumor-promoting potential of mast cells.
Article in Cancer immunology, immunotherapy : CII, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Deciphering the heterogeneity and plasticity of the tumor microenvironment in liver cancer provides insights for prognosis.Frontiers in pharmacology · 2025Article
- Frenemies in the Microenvironment: Harnessing Mast Cells for Cancer Immunotherapy.Pharmaceutics · 2023Review
- KIT as a master regulator of the mast cell lineage.The Journal of allergy and clinical immunology · 2022Review
- Review
- Helicobacter pylori-induced IL-33 modulates mast cell responses, benefits bacterial growth, and contributes to gastritis.Cell death & disease · 2018Article
- Controlling Mast Cell Activation and Homeostasis: Work Influenced by Bill Paul That Continues Today.Frontiers in immunology · 2018Review
- Review
- The Chinese medicine JC-001 enhances the chemosensitivity of Lewis lung tumors to cisplatin by modulating the immune response.BMC complementary and alternative medicine · 2017Article
- Mast Cell-Targeted Strategies in Cancer Therapy.Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie · 2016Review
- HGF/c-MET Axis in Tumor Microenvironment and Metastasis Formation.Biomedicines · 2015Review
- Mast cell plasticity and sphingosine-1-phosphate in immunity, inflammation and cancer.Molecular immunology · 2015Review
- Immunoglobulin free light chains are biomarkers of poor prognosis in basal-like breast cancer and are potential targets in tumor-associated inflammation.Oncotarget · 2014Article
- The roles of mast cells in anticancer immunity.Cancer immunology, immunotherapy : CII · 2012Review
- Mast cells: an expanding pathophysiological role from allergy to other disorders.Naunyn-Schmiedeberg's archives of pharmacology · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mast cells may have either antitumor or tumor-promoting potential. Nevertheless, mast cells in tumor microenvironment have been found to promote tumor growth. So far the mechanisms underlying the modulation of mast cell function in tumor microenvironment remains to be fully elucidated. Here, we report that tumor-promoting potential of mast cells could be augmented by molecules released from damaged tumor cells through cooperative stimulation of stem cell factor (SCF) and ligand for Toll-like receptor 4 (TLR4). Co-simulation with SCF and TLR4 ligand inhibited mast cell degranulation, but efficiently induced the production and secretion of VEGF, PDGF, and IL-10. Although TLR4 ligand alone may induce IL-12 expression in mast cells, co-stimulation with SCF and TLR4 ligand induced the expression of IL-10, but not IL-12, in mast cells. The phosphorylation of GSK3β was crucial for the effect of SCF and TLR4 ligand. In addition to inducing phosphorylation of GSK3β at Ser9 through PI3K pathway, SCF and TLR4 ligand cooperated to induce phosphorylation of GSK3β at Tyr216 by simultaneous activation of ERK and p38MAPK pathways. Both phospho-Ser9 and phospho-Tyr216 of GSK3β were required for IL-10 expression induced by SCF/TLR4 ligand, whereas suppressive effect of SCF/TLR4 ligand on mast cell degranulation was related to phospho-Tyr216. Importantly, the effect of SCF and TLR4 ligand on mast cells could be abrogated by inhibiting phosphorylation of GSK3β at Tyr216. These findings disclose the mechanisms underlying the modulation of mast cell function in tumor microenvironment, and suggest that inhibiting GSK3β in mast cells will be beneficial to the treatment of cancer.
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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 Socratic graph.