Fig. 4: FOXO3a plays a critical role in sorafenib-induced autophagy and knockout of FOXO3a significantly enhances the cytotoxicity of sorafenib to HCC cells. | Cell Death & Disease

Fig. 4: FOXO3a plays a critical role in sorafenib-induced autophagy and knockout of FOXO3a significantly enhances the cytotoxicity of sorafenib to HCC cells.

From: Hypoxia induces sorafenib resistance mediated by autophagy via activating FOXO3a in hepatocellular carcinoma

Fig. 4

A Detection of relative cell viability of sorafenib-treated HCC cells (Huh-7, LM-3, SNU-387, and SNU-449) and sorafenib-treated HCC cells transfected with scramble siRNA (si-NC) and FOXO3a-siRNA (si-FOXO3a; si-NC vs. si-FOXO3a, ***p < 0.001, **p < 0.01; two-way ANOVA). B Western blot analysis of p62 and LC-3 in sorafenib-treated HCC cells (Huh-7, LM-3, SNU-387, and SNU-449) and sorafenib-treated HCC cells transfected with si-NC and si-FOXO3a. C Representative images of autophagic flux detected by fluorescence microscope and mean number of yellow dots (autophagosome) and free red dots (autolysosome) per sorafenib-treated HCC cells (Huh-7, LM-3, SNU-387, and SNU-449) and sorafenib-treated HCC cells transfected with si-NC and si-FOXO3a (si-NC vs. si-FOXO3a, *p < 0.05, #p < 0.05; t-test). D Transmission electron microscope image patterns of autophagosome (marked by red arrows; the right panels are the amplified image of the red frames of left panels) of sorafenib-treated HCC cells (Huh-7, LM-3, SNU-387, and SNU-449) and sorafenib-treated HCC cells transfected with si-NC and si-FOXO3a. Each experiment was performed in triplicate (N = 3). The data are presented as the means ± SD.

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