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. 2021 Jun 3;22(11):6033. doi: 10.3390/ijms22116033

Figure 2.

Figure 2

Inhibition of V600EBRAF activates the AMPK pathway and inhibits mTOR in thyroid cancer cells. Phosphorylation levels of AMPK (p-AMPK), ACC (p-ACC), LKB1 (p-LKB1) and S6 (p-S6), together with total protein levels of AMPK and LKB1 in 8505C and BHT101 cells treated with DMSO (-) or PLX4720 (PLX) (A) or U0126 (U0) (C) for 24 h. (B) p-AMPK, p-ACC, p-S6 and total AMPK levels in cells transfected with a scrambled oligo control (sc) or a specific siRNA for BRAF (siBRAF) for 72 h. (D) p-AMPK, p-ACC and p-S6 expression levels in cells incubated with DMSO or PLX4720, alone or with Dorsomorphin, for 24 h. (E) Expression of LKB1 and p-ACC in cells transfected with an oligo control or specific siRNA for LKB1 (siLKB1) for 48 h, and then incubated in the absence or presence of PLX4720 for 24 h. (F) p-S6 levels in cells incubated with DMSO or PLX4720, in the absence or presence of Rapamycin, for 24 h. (G) Levels of p-AMPK, AMPK, p-S6, HA-BRAF and phosphorylated ERK (p-ERK) in both WRO-mock (-) and WRO-VE (VE) cells treated with DMSO or PLX4720 for 24 h. For each experiment, membranes were reprobed with anti-β-Tubulin as a loading control. Blots are representative of experiments performed three times with similar results.