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. 2020 Mar 27;10:348. doi: 10.3389/fonc.2020.00348

Figure 4.

Figure 4

NiPT induces autophagy through AMP-activated protein kinase–mechanistic target of rapamycin (AMPK-mTOR) and endoplasmic reticulum (ER) stress pathways in lung cancer cells. (A) A549 and NCI-H1299 cells were treated with various concentrations of NiPT, 100 nM bortezomib, and 1 μM b-AP15 for 12 h. The expression levels of p-AMPK, p-mTOR, p-P70S6K S6, and p-S6 were analyzed by immunoblotting. (B) A549 and NCI-H1299 cells were treated with 5 μM NiPT for the indicated time points. The expression levels of p-AMPK, p-mTOR, p-P70S6K S6, and p-S6 were analyzed by immunoblotting. (C) A549 and NCI-H1299 cells were treated with various concentrations of NiPT for 12 h. The expression levels of ATF4, C/EBP-homologous protein (CHOP), and p-eIF2a were analyzed by immunoblotting. (D) A549 and NCI-H1299 cells were treated with 5 μM NiPT for the indicated time points. The expression levels of ATF4, CHOP, and p-eIF2a were analyzed by immunoblotting. (E) A549 cells were treated with or without 5 μM NiPT and bafilomycin (10, 50, 100 nM) for 12 h. The expression levels of calnexin, ATF4, LC3, and p62 were analyzed by immunoblotting.