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. 2016 Aug 23;8(52):89552–89565. doi: 10.18632/oncotarget.11533

Figure 5. Periostin activates EGFR-Akt and EGFR-Erk-c-Myc signaling to regulate the activity of pancreatic cancer cells.

Figure 5

(A) SW1990 and BxPC-3 cells were treated with the supernatant of control shRNA-transfected PSCs (Control sh), periostin shRNA1-transfected PSCs (Periostin sh1), periostin shRNA2-transfected PSCs (Periostin sh2), DMSO (Mock), or human recombinant protein (rPeriostin). After 12 h, cells were harvested and the basal expression of EGFR, Erk, and their downstream molecules was determined by western blotting. (B) Xenograft tumors of nude mice from the control-shRNA group and periostin-shRNA group were also subjected to western blotting using the indicated antibodies. (C) SW1990 and BxPC-3 cells were treated with DMSO, rPeriostin, EGFR inhibitor (Erlotinib, 20 μM), or rPeriostin plus Erlotinib. Cells were harvested at 0, 1, 3, and 6 h, and the basal expression of EGFR, Erk, and their downstream molecules was determined by western blotting. (D) SW1990 and BxPC-3 cells were treated with DMSO, rPeriostin, Erk inhibitor (SCH772984, 20 μM), or rPeriostin plus SCH772984. Cells were harvested after 0, 1, 3, and 6 h, and the basal expression of EGFR, Erk, and their downstream molecules was determined by western blotting.