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. 2015 Oct 15;6(37):39924–39940. doi: 10.18632/oncotarget.5442

Figure 2. In vitro and in vivo characterization of the effect of eIF4H knockdown in A549 cells.

Figure 2

A. Expression analysis of eIF4H and β-actin (loading control) in either A549 wild type (WT) cells or stable clones expressing scrambled shRNA (sh SCR) or eIF4H-targeting shRNA (sh1-4H and sh2-4H). B. Caspase 3/7 activity induction after 8 hours treatment with etoposide (25 μM) or cisplatin (50 μM) in A549 cells expressing eIF4H (sh1 and sh2) or scrambled shRNA. C. PARP cleavage analysis by immunoblotting. A549 cells expressing eIF4H (sh1 and sh2) or scrambled shRNA were untreated or treated for 8 hours with etoposide (25 μM) or cisplatin (50 μM). Full length and typical PARP cleavage were detected. β-actin was used as a loading control. D. Cell proliferation of A549 cells stably expressing or scrambled shRNA under low serum conditions (0.5%) over 7 days using MTT. E. and F. Cell cycle analysis of A549 cells expressing eIF4H sh1 (E) or eIF4H sh2 (F) and scrambled shRNA was carried out using flow cytometry. G. Migration of A549 cells transfected with scrambled shRNA or eIF4H-targeting shRNA was measured in a Boyden chamber assay. Fold induction represent the average number of cells/field in the sh4H-expressing cells over control cells (Scr). H. Tumor volumes measured at indicated time points after subcutaneous injection of eIF4H-deficient or control A549 cells into 10 nude mice in each group. Error bars show SEM.