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. 2017 Aug 3;8(55):93530–93540. doi: 10.18632/oncotarget.19873

Figure 3. Effects of Leptin/LEPR on cell proliferation, survival and migration are mediated via the JAK2/STAT3 pathway.

Figure 3

(A) Proliferation assay. Cell counts over a period of 3 days for the cells indicated either untreated (–) or treated with 100 ng/ml leptin (Lep), with or without specific inhibitors for STAT3 (S3I) or JAK2 (J2I), as indicated. The graph represents the mean and SEM of three independent experiments (*p<0.05). (B) Apoptosis assay. Percentage of apoptosis for the indicated cell lines when treated with sodium azide alone, or with leptin (Lep) treatment, in the presence or absence of inhibitors for STAT3 (S3I) and JAK2 (J2I). The graph shows mean and SEM (n=3; *p<0.05 compared to untreated; **p<0.05 compared to leptin treated). (C) Migration assay. Percentage of wound closure for the indicated cell lines, either untreated (–) or treated with 100 ng/ml leptin (Lep), in the presence or absence of inhibitors for STAT3 (S3I) or JAK2 (J2I), as indicated, showing mean and SEM (*p<0.05).