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. 2021 Mar 15;124(10):1711–1723. doi: 10.1038/s41416-021-01294-0

Fig. 3. Maintenance of mTORC1 hyper-activity in GBM cells upon energy stresses through autophagy-mediated fatty acid oxidation.

Fig. 3

a Lysates were extracted from TSC1 KD LN229 and 2KD LN229 cells treated with BSA or BSA-conjugated palmitate under glc-free conditions for 2 h. The protein levels were examined by western blot using phosphorylated S6RP, total S6RP and vinculin antibodies. Three independent experiments yielded similar results. b Mean ± SE of the ATP content of 2KD LN229 cells treated with BSA or BSA-conjugated palmitate under normal and glc-free conditions for 2 h. n = 5 independent experiments. c Mean ± SE of the ATP content of 400 μM Eto, 400 μM Rano and 2 mM TRMZ-treated LN229 cells in normal media, glc-free media, and 25 mM 2DG media for 2 h were shown. The FAO inhibitors were pre-incubated for 12 h before experiments. n = 5 independent experiments. d Mean ± SE of Max OCR of Eto and TRMZ-treated LN229 cells under normal media, glc-free media, and 25 mM 2DG media treatment conditions were shown. n = 5 independent experiments. e Lysates were extracted from LN229 treated with vehicle, Spautin-1, Eto, and Rano under glc-free and 25 mM 2DG conditions for 2 h. The protein levels were examined by Western blot using antibodies against phosphorylated AMPK, total AMPK, phosphorylated Raptor, total Raptor, phosphorylated S6K, total S6K, phosphorylated S6RP and total S6RP. Three independent experiments yielded similar results. Data were analysed by one-way analysis of variance (ANOVA) with Tukey’s post-hoc test. *p < 0.05, **p < 0.01, ***p < 0.001.