Abstract
Background: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.Methods: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.Results:Interleukin-22 and its receptor were expressed in 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.Conclusions: Interleukin-22 produced by CAFs promotes gastric cancer cell invasion via STAT3 and ERK signalling.
| Original language | English |
|---|---|
| Pages (from-to) | 763-771 |
| Number of pages | 9 |
| Journal | British Journal of Cancer |
| Volume | 111 |
| Issue number | 4 |
| DOIs | |
| State | Published - 2014/08/12 |
Keywords
- ERK
- IL-22
- STAT3
- cancer-associated fibroblast
- gastric cancer
- invasion
ASJC Scopus subject areas
- Oncology
- Cancer Research