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. 2017 Jun 28;8(44):76116–76128. doi: 10.18632/oncotarget.18814

Figure 5. CAFs activated JAK2/STAT3 signaling in lung cancer cells.

Figure 5

Lung cancer cells were cultured with DMEM, CAF-CM, CAF-CM + JAK2 inhibitor AG490 (100 μM) or DMEM + STAT3 inhibitor STATIC (7.5 μM) for 24 h. (A) Protein expression were detected by Western blot. (B) mRNA expression were detected by qPCR. (C) Lung cancer cells were cultured with DMEM, CAF-CM, CAF-CM + JAK2 inhibitor AG490 (100 μM) or DMEM + STAT3 inhibitor STATIC (7.5 μM) for 24 to 48 h. Cell migration ability was measured by wound healing assays. (D) Relative adhension rates at 48 h time point were presented. (E) Lung cancer cells were cultured with DMEM, CAF-CM, CAF-CM + antiIL-6 or DMEM + IL-6 for 24h. mRNA expression were detected by qPCR. (F) Lung cancer cells were cultured with DMEM, CAF-CM, CAF-CM + antiIL-6 or DMEM + IL-6 for 24h. Protein expression were detected by Western blot. Values represent the mean ± SD from three independent experiments. *P<0.05; **P<0.01; ***P<0.001.