@Article{biocell.2019.06352,
AUTHOR = {Xiaoning Qin, Liqing Yuan, Hongxun Ruan, Lin Lin},
TITLE = {Interaction of IL-22/IL-22R1 promotes cell proliferation and suppresses apoptosis of colorectal cancer via phosphorylation of STAT3},
JOURNAL = {BIOCELL},
VOLUME = {43},
YEAR = {2019},
NUMBER = {2},
PAGES = {89--98},
URL = {http://www.techscience.com/biocell/v43n2/33388},
ISSN = {1667-5746},
ABSTRACT = { 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.},
DOI = {10.32604/biocell.2019.06352}
}