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. Author manuscript; available in PMC: 2019 Jul 31.
Published in final edited form as: Bioorg Med Chem. 2017 Mar 23;25(12):2995–3005. doi: 10.1016/j.bmc.2017.03.048

Fig. 4.

Fig. 4.

Compounds impair STAT3 phosphorylation and down-regulate pro-apoptotic Bcl-XL and survivin. (a) Effect of 1 (KIN-1) and 6 (KIN-281) on STAT3, Bcl-XL, and survivin levels as well as STAT3 phosphorylation analyzed by Western blot analysis at several time intervals over the course of 48 h in MDA-MB-468 cells. β-Actin is used as loading control. (b) Quantification of data in (a); the data are presented as percentage changes relative to control (mean ± SD; n = 2). (c) Effect of 1 (KIN-1) and 6 (KIN-281) on STAT3, Bcl-XL, and survivin levels as well as STAT3 phosphorylation analyzed by Western blot analysis at several time intervals over the course of 48 h in MDA-MB-231 cells. β-Actin is used as loading control. (d) Quantification of data in (a); the data are presented as percentage changes relative to control (mean ± SD; n = 2). (e) EMSA analysis to establish STAT3 binding to DNA; lane 1 is (f) Activity of 6 against JAK1, JAK2 and JAK3 kinases. (g) Western blot analysis of Akt phosphorylation as a result of treatment with 1. (h) Quantification of data in (g); the data are presented as percentage changes relative to control (mean ± SD; n = 2).