TY - EJOU AU - Qin, Xiaoning AU - Yuan, Liqing AU - Ruan, Hongxun AU - Lin, TI - Interaction of IL-22/IL-22R1 promotes cell proliferation and suppresses apoptosis of colorectal cancer via phosphorylation of STAT3 T2 - BIOCELL PY - 2019 VL - 43 IS - 2 SN - 1667-5746 AB - Interleukin-22 (IL-22) is a member of IL-10 cytokine family which is expressed in activated T cells predominantly and in activated natural killer cells at lower levels. Previous studies have demonstrated the link between elevated levels of IL-22 and disease severity of psoriasis, Crohn’s disease, rheumatoid arthritis and interstitial lung diseases. However, the function of IL-22 in the development and progression of colorectal cancer (CRC) remains elusive. In this study, we first evaluated the IL-22/IL-22R1 level in CRC patients, and found that tumor tissues have more active expression of IL-22 and IL-22R1 than normal tissues, presenting correlation with the degree of differentiation of tumor tissues. Subsequently, Caspase and cell viability assays were performed on SW-480 cell line which expresses high level of IL-22R1 to examine if the supplementation of IL-22 has an impact on apoptosis and proliferation. In comparison with treatment of 5-FU, supplementation of IL-22 promoted cell proliferation and ameliorated apoptosis. To unveil signal transduction upon activation of IL-22R, we examined the phosphorylation of STAT3 in SW-480 cell line following supplementation of IL-22. The treatment of IL-22 also increased the level of p-Akt, an essential component in PI3K/Akt pathway. Although the link between STAT3 phosphorylation and PI3K/ Akt activation remains to be explored, our study revealed the mechanism underlying the effects of IL-22R activation on apoptosis as well as tumor differentiation, indicating the prognostic value of IL-22/IL-22R. KW - Interleukin-22 KW - Colorectal cancer KW - PI3K/Akt signaling pathway KW - STAT3 DO - 10.32604/biocell.2019.06352