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. 2017 Mar 21;7:45077. doi: 10.1038/srep45077

Figure 6. Inhibition of STAT3 or AKT on keratinocyte survival and proliferation.

Figure 6

(A–C) Effect of inhibition of STAT3 or AKT on DMBA-induced apoptosis in keratinocytes. Primary keratinocytes from both genotypes were pretreated with either STAT3 inhibitor S3I-201 (20 μM) or AKT1/2 inhibitor A6730 (10 μM) for 1 h before DMBA treatment. (A) Representative images of morphological changes of primary keratinocytes from both genotypes following treatment of DMBA for 24 h. (B) Quantitative analysis of percentage of apoptotic cells after 24 h of DMBA treatment. *p < 0.05 by Mann-Whitney U test. Values labelled (A-E) were evaluated against each other by ANOVA; bars designated by the same letter are statistically similar, whereas bars designated with different letters are significantly different, p < 0.05. (C) Caspase-3 activity was measured after 24 h of DMBA treatment. *p < 0.05 by Mann-Whitney U test. Values designated by the same letter are statistically similar, whereas values designated with different letters are significantly different at p < 0.05 as determined by ANOVA. (D–F) Effect of inhibition of STAT3 or AKT on TPA-induced cell proliferation in keratinocytes. Primary keratinocytes from both genotypes were pretreated with either AKT1/2 inhibitor A6730 (10 μM) or STAT3 inhibitor S3I-201 (20 μM) for 1 h before TPA treatment. Following the 1 h pulse treatment of TPA (40 nM), cell proliferation was measured at the indicated time using WST-assay. (D) Inhibition of cell proliferation by S3I-201 (10–50 μM). (E) Inhibition of cell proliferation by STA-21 (0.1–10 μM). (F) Inhibition of cell proliferation by A6730 (0.1–10 μM). Values designated by the same letter are statistically similar, whereas values designated with different letters are significantly different, p < 0.05 determined by ANOVA.