Skip to main content
. 2020 Sep 2;11(8):717. doi: 10.1038/s41419-020-02924-w

Fig. 4. Inhibition of AMPKα/ULK1 mediates cell survival in SH003-treated GC cells.

Fig. 4

a AGS and SNU-638 cells were treated with SH003 (400 μg/mL) for the indicated times. After SH003 treatment, cell lysates were loaded for Western blotting and detected antibodies targeting p-AMPKα (Thr172), AMPKα, p-ULK1 (Ser555), ULK1, p-mTOR (Ser2448), and p-p70S6K (Thr389) for autophagy induction. β-actin was used as a protein loading control. b, c Cell viability, LDH release, and Western blot analyses of p-AMPKα, p-ULK1, LC3B, and cleaved caspase-3 in the AGS and SNU-638 cells treated with SH003 (400 μg/mL, 24 h) in the presence or absence of Compound C (2 μM, 24 h); *p < 0.05. (D-F) Cell viability, LDH release, and Western blot analysis of p-ULK1 and LC3B in the AGS and SNU-638 cells treated with SH003 (400 μg/mL, 24 h) in the presence or absence of SBI-0206965 (10 μM, 24 h); *p < 0.05. (G-I) Cell viability, LDH release and western blot analyses of p-ULK1, LC3B, and cleaved caspase-3 in the AGS and SNU-638 cells treated with SH003 (400 μg/mL, 24 h) in the presence or absence of ULK1 siRNA (30 nM, 24 h); *p < 0.05. β-actin was used as a protein loading control.