ArticleCellular oncology (Dordrecht, Netherlands)2019
CCL18 secreted from M2 macrophages promotes migration and invasion via the PI3K/Akt pathway in gallbladder cancer.
Article in Cellular oncology (Dordrecht, Netherlands), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 41 papers.
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41 citing papers in PubMed, 65 citations in OpenAlex.
- Article
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- Lactate activates CCL18 expression via H3K18 lactylation in macrophages to promote tumorigenesis of ovarian cancer.Acta biochimica et biophysica Sinica · 2024Article
- The Role of Chemokines in Orchestrating the Immune Response to Pancreatic Ductal Adenocarcinoma.Cancers · 2024Review
- MFG-E8 promotes M2 polarization of macrophages and is associated with poor prognosis in patients with gastric cancer.Heliyon · 2024Article
- Unveiling the contribution of tumor-associated macrophages in driving epithelial-mesenchymal transition: a review of mechanisms and therapeutic Strategies.Frontiers in pharmacology · 2024Review
- Improving the therapeutic efficacy of oncolytic viruses for cancer: targeting macrophages.Journal of translational medicine · 2023Review
- Role of chemokines in the crosstalk between tumor and tumor-associated macrophages.Clinical and experimental medicine · 2023Review
- Dynamic changes in macrophage subtypes during lung cancer progression and metastasis at single-cell resolution.Journal of thoracic disease · 2023Article
- ELF3 promotes gemcitabine resistance through PKMYT1/CDK1 signaling pathway in gallbladder cancer.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- Tumour-associated macrophages: versatile players in the tumour microenvironment.Frontiers in cell and developmental biology · 2023Review
- Bacteria and macrophages in the tumor microenvironment.Frontiers in microbiology · 2023Review
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- The extracellular vesicles targeting tumor microenvironment: a promising therapeutic strategy for melanoma.Frontiers in immunology · 2023Review
- Small Molecular Inhibitors Reverse Cancer Metastasis by Blockading Oncogenic PITPNM3.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- CCL18 Expression Is Higher in a Glioblastoma Multiforme Tumor than in the Peritumoral Area and Causes the Migration of Tumor Cells Sensitized by Hypoxia.International journal of molecular sciences · 2022Article
- CCL18 promotes breast cancer progression by exosomal miR-760 activation of ARF6/Src/PI3K/Akt pathway.Molecular therapy oncolytics · 2022Article
- A multi-cellular molecular signaling and functional network map of C-C motif chemokine ligand 18 (CCL18): a chemokine with immunosuppressive and pro-tumor functions.Journal of cell communication and signaling · 2022Article
- Oral Cancer Stem Cell-Derived Small Extracellular Vesicles Promote M2 Macrophage Polarization and Suppress CD4Stem cells international · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
purposeThe presence of M2 macrophages within primary tumors has been correlated with a poor prognosis for many types of cancer. However, little is known about the role of M2 macrophages in gallbladder cancer (GBC).
methodsThe number of M2 macrophages in 78 GBC and 16 normal gallbladder tissue samples was assessed by immunohistochemistry. The THP-1 monocyte cell line was differentiated into M2 macrophages and co-cultured with GBC-derived cell lines. The effect of M2 macrophages on promoting GBC cell migration and invasion was analyzed using migration, invasion and scratch wound healing assays. Western blotting and real-time PCR were used to assess the expression of epithelial-mesenchymal transition (EMT) markers and the activation status of the PI3K/Akt signaling pathway in GBC cells co-cultured with THP-1-derived macrophages.
resultsThe average number of M2 macrophages was found to be significantly higher in GBC tissues than in normal gallbladder tissues. We also found that GBC patients with higher M2 macrophage counts exhibited poorer overall survival rates. Co-culture with M2 macrophages significantly promoted the migration, invasion and EMT of GBC cells. Moreover, we found that CCL18 secreted from M2 macrophages had the same effect on GBC cells as M2 macrophages. Blocking the function of CCL18 with a neutralizing antibody reversed this effect. Finally, we found that M2 macrophages could activate PI3K/Akt signaling in GBC cells, thereby leading to migration, invasion and EMT of these cells.
conclusionsOur findings contribute to our understanding of the role of chronic inflammation in GBC development and progression, and may offer potential therapeutic targets for GBC.
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