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. 2015 Oct 20;6(37):40158–40171. doi: 10.18632/oncotarget.5522

Figure 2. TrkB led to Twist-1 upregulation through activation of the JAK/STAT3 pathway after TrkB/c-Src/JAK2 complex formation.

Figure 2

A. Western blot analysis of expression of phospho-JAK2, JAK2, phospho-STAT3, STAT3, and Twist-1 proteins in Hs578T and MDA-MB-231 cells treated with 5 μM SU6656. β-actin was used as a loading control. B. Western blot analysis of expression of phospho-JAK2, JAK2, phospho-STAT3, STAT3, and Twist-1 proteins in Hs578T and MDA-MB-231 cells treated with 15 μM AG490. β-actin was used as a loading control. C. Identification of complex formation of endogenous TrkB/c-Src/JAK2 in MBA-MB-231 and Hs578T cells. D. Western blot analysis of whole-cell lysates and immunoprecipitates derived from 293T cells transfected with V5-TrkB, HA-c-Src and Myc-Jak2 constructs as indicated with or without 5 μM SU6656. E. The relative expression levels of mRNA encoding Twist-1 and Twist-2 in MDA-MB-231 cells stably expressing control shRNA or TrkB-shRNA treated with or without 5 μM SU6656, as determined by quantitative RT-PCR. F. Western blot analysis of the expression of phospho-JAK2, JAK2, phospho-STAT3, STAT3, and Twist-1 in SYF cells expressing either pCAG or pCAG/TrkB. β-actin was used as a loading control. G. Western blot analysis of expression of phospho-JAK2, JAK2, phospho-STAT3, STAT3, and Twist-1 in SYF cells or SYF-c-Src cells expressing either pCAG or pCAG/TrkB. β-actin was used as a loading control.