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. 2015 May 16;6(25):21085–21099. doi: 10.18632/oncotarget.3912

Figure 5. Involvement of PI3K, ERK and c-MYC in HER3/MUC4 mediated signaling in HER2 knockdown pancreatic cancer cells and tumorigenic properties of HER2 knockdown cells.

Figure 5

A. Western blot results show that PI3K, phosphorylation of ERK and c-Myc were elevated in HER2 knockdown cells than control cells. The increased expression and activity of PI3K, ERK and c-MYC may be involve the HER3/MUC4 mediated signaling in HER2 low expressing pancreatic cancer cells. B. We have also confirmed the involvement of PI3K and c-Myc by PI3k inhibitor NVP-BEZ235 treatment. This finding suggests that hyperproliferation of HER2 knockdown cells is due to downstream activity of PI3K and c-Myc. C. The tumorigenicity assay results indicate that HER2 knockdown pancreatic cancer cells have high tumor weight than control cells injected in mice. D. Corresponding immunostaining of HER2 and HER3 in pancreatic cancer cells (CD18/HPAF scrambled control/CD18/HPAF Sh-HER2 and Capan-1 scrambled control/Capan-1 Sh-HER2) subcutaneous tumors, indicates that HER3 expression is increased in HER2 knockdown tumor tissues (figure magnification 10X).