Fig. 3

Activating the MAPK pathway induces LAT1 expression in a patient with PLNTY. a Immunohistochemistry of indicated proteins in the high-methionine-uptake (#1) and low-methionine-uptake (#2) regions within tumor tissue. Bars, 50 μm. b Western blot analysis of phospho-MEK, phospho-ERK, c-Myc, and LAT1 proteins in YMG83 (PLNTY, left) cells treated with DMSO and 10 μM BRAF inhibitor (BRAFi, dabrafenib) for 12 h. GAPDH, loading control. c Relative cell viability of dabrafenib-treated (left) and trametinib-treated (right) YMG83 cells and immortalized normal human astrocytes (NHA). *P < 0.05, DMSO versus dabrafenib (left) and trametinib (right). d Western blot analysis for indicated proteins in YMG62 (epithelioid glioblastoma, left) and AM-38 (glioblastoma, right) cells treated with DMSO, 10 μM BRAF inhibitor (BRAFi, dabrafenib), and 10 μM MEK inhibitor (MEKi, trametinib) for 24 h. GAPDH, loading control. e Western blot analysis of BRAF, phospho-MEK, phospho-ERK, c-Myc, and LAT1 proteins in YMG62 (left) and AM-38 (right) cells treated with DMSO and dabrafenib at indicated concentrations. Vinculin, loading control. f Western blot analysis for indicated proteins in non-silencing- (NS) and BRAF- (#1 and #2) transduced YMG62 and AM38 cells. GAPDH, loading control