Fig. 6

TGF-β2 and autophagy-mediated energy generation of glioma and mitochondria function. a Control or autophagy inhibited tumor groups with or without TGF-β2 treatment (10 ng/ml, 24 h) were stained with MitoTracker Red and classified as three forms (Scale bars, 50 μm). Percentages of the different morphologies were assessed. b Mitochondria trafficking capacity were divided by the distance from the mitochondria to nuclei visualized by MitoTracker Red and then were classified shown by the representative images (scale bars, 50 μm). Percentages were also calculated. c JC-1 probe was added to NTC and Baf-treated tumor cells with or without added TGF-β2 to test the mitochondrial membrane potential (△Ψm). d The quantitative analysis of △Ψm was conducted by flow cytometry (one-way ANOVA, columns: percentage of low △Ψm cells). e Immunoblots presented mitochondria fussion/fission related markers affected by TGF-β and Baf (Student’s t-test; Columns, ratio of P-Drp1/Drp1. Bars, SD. *, P < 0.05; **, P < 0.01). f OCR and ECAR in normal and autophagy cells inhibited with or without TGF-β2 treatment. OCR and ECAR were measured using the XF24 Seahorse Analyzer. g, h ATP and L-lactate levels were significantly increased upon treatment with TGF-β2.and baf treatment attenuated this effect, as examined using an ATP and L-lactate kit assay (Student’s t-test; Columns, means of triplicate assays. Bars, SD. *, P < 0.05; ***, P < 0.001)