Skip to main content
Fig. 6 | Cancer Cell International

Fig. 6

From: TAZ inhibition promotes IL-2-induced apoptosis of hepatocellular carcinoma cells by activating the JNK/F-actin/mitochondrial fission pathway

Fig. 6

TAZ modulates mitochondrial fission via the JNK/F-actin pathway. a–c Western blotting was used to analyze JNK activity and F-actin expression. IL-2 treatment promoted JNK phosphorylation and F-actin upregulation; this effect was further enhanced by TAZ deletion. To inhibit the activity of JNK, SP600125 (SP) was added to TAZ-depleted cells. To activate the JNK pathway, anisomycin (Ani) was added to control cells. d, e Immunofluorescence staining of phosphorylated JNK following TAZ deletion and IL-2 treatment. f, g Immunofluorescence staining for F-actin following JNK activation or inhibition. h, i Immunofluorescence staining of mitochondria. The average number of mitochondria was recorded. *P < 0.05 vs. control (Ctrl) group; #P < 0.05 vs. IL-2 group; @P < 0.05 vs. IL-2 + si-TAZ group

Back to article page