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. 2012 Aug 21;41(5):1577–1586. doi: 10.3892/ijo.2012.1594

Figure 2.

Figure 2.

IL-22 induces transient STAT3 phosphorylation and the phosphorylation of several members of the MAPK pathways in MISK81-5, oral squamous cell carcinoma cells. (A) MISK81-5 and (B) HSC-3 cells were incubated with IL-22 (20 ng/ml) or IL-6 (20 ng/ml) for varying times up to 120 min. (A) IL-22 and IL-6 induced pY705-STAT3 in MISK81-5 cells within 15 and 5 min, respectively. IL-22 induced transient tyrosine phosphorylation of STAT3 in MISK81-5 cells with similar kinetics to IL-6. IL-22 and IL-6 induced subtle changes in pS727-STAT3 within the tested time periods. IL-22 induced a transient activation of ERK1/2 in MISK81-5 cells and also induced a delayed phosphorylation of p38 MAP kinase, similar to IL-6. (B) In HSC-3 cells, pY705-STAT3 was undetectable after IL-22 stimulation, although transient pY705-STAT3 expression was induced after IL-6 stimulation. IL-22 and IL-6 induced the transient serine phosphorylation of STAT3. HSC-3 cells stimulated with IL-6 showed activation of ERK1/2 and p38 MAP kinases similar to that in MISK81-5 cells. However, the activation in HSC-3 cells was undetectable after IL-22 treatment. All findings represent the results of three independent experiments.