NOX4-Derived ROS Mediates TGF-β1-Induced Metabolic Reprogramming during Epithelial-Mesenchymal Transition through the PI3K/AKT/HIF-1α Pathway in Glioblastoma

Figure 4

TGF-β1 induces epithelial-to-mesenchymal transition and proliferation, migration, and invasion via NOX4/ROS signal pathway of glioblastoma cells. (a) Western blot analysis showed the time-dependent effects of EMT markers under TGF-β1 treatment (10 ng/ml) on glioblastoma cells. (b) Western blot analysis of EMT markers when NOX4 was suppressed and deleted under TGF-β1 treatment (10 ng/ml) for 24 hours on glioblastoma cells. (c) Immunofluorescences observed Vimentin expression in glioblastoma cells after treated with TGF-β1.  μm. (d) CCK-8 assays were performed to evaluate the glioblastoma cell’s viability and growth. (e) EdU proliferation assays were performed to evaluate the growth of glioblastoma cells. The EdU incorporation was quantitated.  μm. (f) Crystal violet stained sections of the Matrigel matrix. Migration and invasion ability of glioblastoma cells were determined by transwell assay. The average number of migrating and invading cells was counted after 24 hours of migration and invasion.  μm. Data represent mean and SD of three independent experiments. ; ; .

(a)

(b)

(c)

(d)

(e)

(f)