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. 2018 May 29;9(6):649. doi: 10.1038/s41419-018-0658-y

Fig. 7. Autophagy inhibition suppresses DSGOST-induced EMT phenomenon in gastric cancer.

Fig. 7

a AGS cells were treated with DSGOST (500 μg/mL, 24 h) in the absence or presence of 3-MA (5 mM, left) and CQ (10 µM, right). Extracted proteins were subjected to western blotting using antibody for EMT markers, such as E-cadherin, N-cadherin, vimentin, Slug, Snail, and LC3B. b Real-time RT-PCR was performed using primers for E-cadherin and β-actin in DSGOST (500 μg/mL, 24 h)- and/or 3-MA (5 mM, 24 h)-treated AGS cells. c AGS cells were transfected with a reporter luciferase vector (pGL2) containing E-cadherin promoter (−368~+51) and treated with DSGOST (500 μg/mL, 24 h) and/or 3-MA (5 mM, 24 h). *p < 0.05. d, e After transfection by LC3B or Beclin-1 siRNA in AGS and SNU-638 cells, these cells were treated with/without DSGOST (500 μg/mL, 24 h). Extracted proteins were subjected to western blotting using antibodies for EMT markers, including E-cadherin, N-cadherin, Slug, Snail, and LC3B. β-actin was used as the protein loading control