Propolin C Inhibited Migration and Invasion via Suppression of EGFR-Mediated Epithelial-to-Mesenchymal Transition in Human Lung Cancer Cells

Figure 6

Degeneration of EGF-induced EMT via PI3K/Akt and ERK inhibition in propolin C-treated A549 lung cancer cells. A549 cells were synchronized and (a) pretreated with propolin C (2.5, 5, 7.5, and 10 μM) or (b) pretreated with 10 μM of propolin C (PPC) for 30 min and then stimulated with 50 ng/mL EGF for 5, 15, and 30 min. After EGF incubation, cell lysates were harvested and Western blot analyses were then performed to detect the expressions of E-cadherin, vimentin, slug, snail, phospho-ERK, ERK, phospho-Akt, Akt, and β-actin. Significant difference was observed from the compared groups ( < 0.05). (c) HCC827 cells were pretreated with propolin C (PPC, 10 μM), LY294002 (LY, 10 μM), and PD98059 (PD, 10 μM) alone or cotreated with LY294002 or PD98059 with propolin C for 30 min and then incubated with EGF (50 ng/mL) for 24 h. After incubation, cells were harvested and Western blot analyses were used to detect E-cadherin, vimentin, snail, slug, and β-actin expressions. Data were shown as mean ± SD (). Different uppercase letters (A−D) indicate statistical differences among group (), and the same letter showed no difference ().

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