Fig. 4
From: DRP2 promotes EMT and serves as a potential therapeutic target for LUAD treatment
DRP2 knockdown inhibited EMT in A549 and H1299 cells. (A–C) The expression levels of DRP2 in bronchial epithelial cells (BEAS-2B) and various NSCLC cell lines (including A549, H1299, H1650, and H226) were analyzed through qRT-PCR (A) and Western blotting (B,C) methodologies, with β-actin protein utilized as the internal reference for standardization in these assessments. (D–F) The expression of EMT markers was detected by qRT-PCR (D) and western blotting (E,F). (G,H) The wound-healing assay was conducted utilizing DRP2-knockdown cells, alongside control cells. The extent of wound closure at 0 and 24 h post-initiation was quantitatively assessed. (I,J) Transwell assay was used to detect the migration and invasion ability of knockdown and control DRP2 cells. Count the number of cells in the field of view after crystal violet staining. Each experiment was performed three times and the data were expressed as mean ± standard deviation (SD, n = 3). *P < 0.05, **P < 0.01, ***P < 0.001 versus “sh-NC” group. Scale bar = 100 μm.
