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. 2018 Jun 13;9(6):703. doi: 10.1038/s41419-018-0735-2

Fig. 5. Silencing ANO1 activates TNF-α downstream signaling by phosphorylation of FADD and activation of caspase family members for induction of apoptosis.

Fig. 5

a–c Silencing of endogenous ANO1 promotes phosphorylation of FADD. Left panel of (a), Immunoblots of lysates from PC-3 cells transfected with ANO1-siRNAs or NCsi for 72 h. Right panel of (a), Immunoblots of lysates from normal RWPE-1 cells stably expressing ANO1 or the IRES2-GFP vector as the control. Bar graph showing quantitative analysis of phospho-FADD and total FADD protein expression in PC-3 cells with ANO1 knockdown (b: n = 4) and RWPE-1 cells with ANO1 overexpression (c: n = 3) from (a). d, e Silencing of endogenous ANO1 promotes the expression of caspases. Immunoblots of lysates from PC-3 cells transfected with ANO1-siRNAs or NCsi for 72 h. Bar graph showing quantitative analysis of protein expressions (e n = 4) from (d). Data were normalized to NC group cells. f, g Human TNF-α antibody reduces caspase-7 overexpression induced by ANO1 knockdown in PC-3 cells. Bar graph showing quantitative analysis of caspase-7 protein expressions (g n = 4, **p < 0.01 vs NC) from (f)