Journal: Frontiers in Molecular Biosciences

Article Title: Mechanistic study of glutamine metabolic reprogramming driving non-small cell lung cancer progression via the FGF17-FGFR4 axis mediating epithelial-mesenchymal transition

doi: 10.3389/fmolb.2025.1728698

Figure Lengend Snippet: Verify that glutamine metabolism acts on MEK5/ERK5 through the FGF17-FGFR4 axis to affect the oxidative stress level and apoptosis in NCI-H1299 cells. (A) Western blot analysis on the protein expression of E-cadherin, Vimentin, FGF17, FGFR4, p-MEK5, MEK5, p-ERK5, and ERK5 in NCI-H1299 cells (The blot for tubulin is shown once as it serves as the loading control for both GLUL and the above proteins, which were derived from the same cell samples); (B) Effect of FGF17 silencing and glutamine deprivation on ECAR and OCR in NCI-H1299 cells; (C) JC-1 mitochondrial membrane potential assay in NCI-H1299 (scale bar = 100 μm); (D) Quantitative results of the JC-1 mitochondrial membrane potential assay by ImageJ; (E) The effects of FGF17 silencing and glutamine deprivation on GSH/GSSG levels in NCI-H1299; (F) DCFH-DA assay to assess ROS level in NCI-H1299 (scale bar = 100 μm); (G) Quantitative results of the DCFH-DA assay by ImageJ. (Quantitative data are expressed as Mean ± SD, with three samples at least per group. For comparisons with Ctrl groups, ns, no significance; * p < 0.05, ** p < 0.01, *** p < 0.001).

Article Snippet: Commercialized diagnostic test kits, including fluorogenic probe H2DCFDA (HY-D0940, MCE), GSH/GSSG Assay Kit (HY-K0311, MCE), JC-1 mitochondrial membrane potential assay kit (HY-K0601, MCE), were employed to assess metabolic and redox parameters in NCI-H1299 cells or mice tutors tissue homogenates.

Techniques: Western Blot, Expressing, Control, Derivative Assay, Membrane, DCFH-DA Assay

Journal: Frontiers in Molecular Biosciences

Article Title: Mechanistic study of glutamine metabolic reprogramming driving non-small cell lung cancer progression via the FGF17-FGFR4 axis mediating epithelial-mesenchymal transition

doi: 10.3389/fmolb.2025.1728698

Figure Lengend Snippet: Impact of FGF17 knockdown and cisplatinum on tumor growth in tumor-bearing mice. (A) Dissection images of subcutaneous xenograft mice in each group ( n = 5); (B) Tumor volume and weight in subcutaneous xenograft mice ( n = 5); (C) The levels of glutamine, GSH/GSSG ratio, and ROS in the tumors of each group of mice; (D) Representative image of E-cadherin immunofluorescence (scale bar = 100 μm); (E) Representative image of Vimentin immunofluorescence (scale bar = 100 μm); (F) Quantitative results of immunofluorescence for E-cadherin and Vimentin proteins by ImageJ; (G) Western blot analysis on the protein expression of E-cadherin, Vimentin, FGF17, FGFR4, p-MEK5, MEK5, p-ERK5, and ERK5 in mice; (H) Quantitative results of Western blot analysis by ImageJ. (Quantitative data are presented as the Mean plus or minus the Standard Deviation, with a minimum of three samples for each group. When making comparisons with the PDX group, a single asterisk (*) indicates p-value less than 0.05, double asterisks (**) denote p-value less than 0.01, and triple asterisks (***) signify p-value less than 0.001).

Article Snippet: Commercialized diagnostic test kits, including fluorogenic probe H2DCFDA (HY-D0940, MCE), GSH/GSSG Assay Kit (HY-K0311, MCE), JC-1 mitochondrial membrane potential assay kit (HY-K0601, MCE), were employed to assess metabolic and redox parameters in NCI-H1299 cells or mice tutors tissue homogenates.

Techniques: Knockdown, Dissection, Immunofluorescence, Western Blot, Expressing, Standard Deviation