ArticleBritish journal of cancer2014
IL-22 produced by cancer-associated fibroblasts promotes gastric cancer cell invasion via STAT3 and ERK signaling.
Article in British journal of cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 87 citations in OpenAlex.
- Review
- Cytokines and cancer-associated fibroblasts.Journal of hematology & oncology · 2026Review
- Fibroblasts selectively modulate immune cell-derived cytokine effects on tumor cells in colorectal cancer.Frontiers in immunology · 2026Article
- Evaluating IL22RA1 expression as a predictive indicator in human colon cancer progression.BMC cancer · 2025Article
- Crosstalk between cancer‑associated fibroblasts and inflammation in tumor microenvironment: A novel perspective in cancer therapy (Review).Oncology reports · 2025Review
- IL-20 Subfamily Biological Effects: Mechanistic Insights and Therapeutic Perspectives in Cancer.International journal of molecular sciences · 2025Review
- ERK1/2 Signaling in Intrahepatic Cholangiocarcinoma: From Preclinical Advances to Therapeutic Strategies.Biology · 2025Review
- Interleukin-22 promotes endometrial carcinoma cell proliferation and cycle progression via ERK1/2 and p38 activation.Molecular and cellular biochemistry · 2025Article
- IL-22/IL-22R1 pathway enhances cholangiocarcinoma progressionWorld journal of gastrointestinal oncology · 2025Article
- The role of transcription factors in the crosstalk between cancer-associated fibroblasts and tumor cells.Journal of advanced research · 2025Review
- The role of IL-22 in cancer.Medical oncology (Northwood, London, England) · 2024Review
- Cancer associated fibroblasts and metabolic reprogramming: unraveling the intricate crosstalk in tumor evolution.Journal of hematology & oncology · 2024Review
- Role of IL-22 in intestinal microenvironment and potential targeted therapy through diet.Immunologic research · 2023Review
- Comprehensive pan-cancer analysis of STAT3 as a prognostic and immunological biomarker.Scientific reports · 2023Article
- MAPK4 silencing in gastric cancer drives liver metastasis by positive feedback between cancer cells and macrophages.Experimental & molecular medicine · 2023Article
- T cell-derived interleukin-22 drives the expression of CD155 by cancer cells to suppress NK cell function and promote metastasis.Immunity · 2023Article
- Signaling pathways and therapeutic interventions in gastric cancer.Signal transduction and targeted therapy · 2022Review
- Inflammatory Cytokine: An Attractive Target for Cancer Treatment.Biomedicines · 2022Review
- Inflammation and Gastric Cancer.Diseases (Basel, Switzerland) · 2022Review
- The Impact of Obesity, Adipose Tissue, and Tumor Microenvironment on Macrophage Polarization and Metastasis.Biology · 2022Review
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInterleukin-22 (IL-22) has been recently highlighted owing to its biological significance in the modulation of tissue responses during inflammation. However, the role of IL-22 in carcinogenesis has remained unclear. Here, we investigated the pathophysiological significance of IL-22 expression in gastric cancer tissues and examined the mechanism by which IL-22 promotes gastric cancer cell invasion.
methodsHuman gastric cancer specimens were analysed by immunohistochemistry for expression of IL-22 and IL-22 receptor 1 (IL-22R1). The effects of IL-22-induced STAT3 and ERK signalling on invasive ability of gastric cancer cells were examined using a small-interfering RNA system and specific inhibitors. AGS cells were co-cultured with cancer-associated fibroblasts (CAFs) from human gastric cancer tissues and assessed by invasion assay.
resultsInterleukin-22 and its receptor were expressed in α-smooth muscle actin-positive stromal cells and tumour cells at the invasive front of gastric cancer tissues, respectively. The expression of IL-22 and IL-22R1 was significantly related to lymphatic invasion. Interleukin-22 treatment promoted the invasive ability of gastric cancer cells through STAT3 and ERK activation. The invasive ability of gastric cancer cells was significantly enhanced by co-culture with IL-22-expressing CAFs.
conclusionsInterleukin-22 produced by CAFs promotes gastric cancer cell invasion via STAT3 and ERK signalling.
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