IL-22 produced by cancer-associated fibroblasts promotes gastric cancer cell invasion via STAT3 and ERK signaling

Interleukin-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 gas...

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Bibliographic Details
Published in:British journal of cancer 2014-08, Vol.111 (4), p.763-771
Main Authors: FUKUI, H, ZHANG, X, IMURA, J, FUJIMORI, T, SASAKO, M, MIWA, H, SUN, C, HARA, K, KIKUCHI, S, YAMASAKI, T, KONDO, T, TOMITA, T, OSHIMA, T, WATARI, J
Format: Article
Language:English
Subjects:
Adult
Aged
Aged, 80 and over
Antibodies
Biological and medical sciences
Cell Line, Tumor
Cells
Coculture Techniques
Cytokines
Female
Fibroblasts
Fibroblasts - metabolism
Gastric cancer
Gastroenterology. Liver. Pancreas. Abdomen
Humans
Inflammation
Interleukin-22
Interleukins - metabolism
Internal medicine
Male
MAP Kinase Signaling System
Medical sciences
Medicine
Metastasis
Middle Aged
Molecular Diagnostics
Multiple tumors. Solid tumors. Tumors in childhood (general aspects)
Neoplasm Invasiveness
Phosphorylation
Protein Processing, Post-Translational
Receptors, Interleukin - metabolism
STAT3 Transcription Factor - metabolism
Stomach Neoplasms - metabolism
Stomach Neoplasms - pathology
Stomach. Duodenum. Small intestine. Colon. Rectum. Anus
Tumors
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Summary:Interleukin-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. Human 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. Interleukin-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. Interleukin-22 produced by CAFs promotes gastric cancer cell invasion via STAT3 and ERK signalling.
ISSN:0007-0920
1532-1827
DOI:10.1038/bjc.2014.336