ArticleGastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association2017
Site-specific fibroblasts regulate site-specific inflammatory niche formation in gastric cancer.
Article in Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 12 citations in OpenAlex.
- Novel immunotherapy for gastric cancer: targeting the CD47-SIRPα axis.Cancer metastasis reviews · 2025Review
- CPT1C-positive cancer-associated fibroblast facilitates immunosuppression through promoting IL-6-induced M2-like phenotype of macrophage.Oncoimmunology · 2024Article
- CCL13 and human diseases.Frontiers in immunology · 2023Review
- Cancer-associated fibroblasts refine the classifications of gastric cancer with distinct prognosis and tumor microenvironment characteristics.Frontiers in oncology · 2023Article
- The Interplay of Four Main Pathways Recomposes Immune Landscape in Primary and Metastatic Gastroenteropancreatic Neuroendocrine Tumors.Frontiers in oncology · 2022Article
- Weighted Gene Co-expression Network Analysis Identifies a Cancer-Associated Fibroblast Signature for Predicting Prognosis and Therapeutic Responses in Gastric Cancer.Frontiers in molecular biosciences · 2021Article
- Role of Cancer-Associated Fibroblast in Gastric Cancer Progression and Resistance to Treatments.Journal of oncology · 2019Review
- Molecular alterations of cancer cell and tumour microenvironment in metastatic gastric cancer.Oncogene · 2018Review
- Priming in response to pro-inflammatory cytokines is a feature of adult synovial but not dermal fibroblasts.Arthritis research & therapy · 2017Article
- Expression of Helios in gastric tumor cells predicts better survival in gastric cancer patients.Journal of cancer research and clinical oncology · 2016Article
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6 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundFibroblasts are the commonest type of cancer stromal cells. Inflammation occurs in cancer tissue, and the inflammatory process has been suggested to be caused by interactions between immune cells and cancer cells. In this study, we clarified that site-specific fibroblasts regulate the formation of a site-specific inflammatory niche according to the depth of gastric cancer cell invasion.
methodsImmunohistochemistry was performed with paraffin-embedded tissues. The numbers of immune cells and the fibroblast area were calculated according to the cancer depth. The gene expression patterns of submucosal fibroblasts and subperitoneal fibroblasts stimulated with HSC44PE-conditioned medium were analyzed with a microarray. To examine the effects on the cancer microenvironment of differences in gene expressions between HSC44PE-stimulated submucosal fibroblasts and subperitoneal fibroblasts, assays of HSC44PE proliferation, T cell migration, and M2-like macrophage differentiation were performed.
resultsThe distributions of immune cells differed between the submucosal layer and the subserosal layer. The number of M2 macrophages was significantly higher and the fibroblast area was significantly larger in the subserosal layer compared with the submucosal layer. High expression levels of IL1B, TNFSF15, and CCL13 were observed in HSC44PE-stimulated submucosal fibroblasts, and higher expression levels of TGFB2, CSF1, CCL8, and CXCL5 were found in HSC44PE-stimulated subperitoneal fibroblasts. HSC44PE-stimulated subperitoneal fibroblast medium promoted the differentiation of monocytes into M2-like macrophages, whereas HSC44PE-stimulated submucosal fibroblasts significantly induced the migration of Jurkat cells and the growth of HSC44PE cells.
conclusionThe dynamic states of immune cells differ between the submucosal and subserosal layers in cancer tissues. Site-specific fibroblasts regulate site-specific inflammatory niche formation according to the depth of cancer cell invasion.
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