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Fig. 5. Arctigenin-induced FaDu pharyngeal carcinoma cell death is meditated by both intrinsic and extrinsic pathways. (A) Extrinsic death receptor-mediated apoptotic signaling pathway induced by Arctigenin. Arctigenin upregulated the expression level of the death receptor ligand Fas and subsequently activated the extrinsic death receptor-mediated apoptotic signaling pathway through the cleavage of caspase-8 in FaDu cells. (B) Intrinsic mitochondria-dependent apoptotic signaling pathway induced by Arctigenin. Arctigenin downregulated anti-apoptotic factors Bcl-2 and Bcl-xL associated with the intrinsic mitochondria-dependent apoptotic pathway and upregulated the mitochondria-dependent pro-apoptotic factors Bax and Bad in FaDu cells. (C) Extrinsic death receptor-mediated and intrinsic mitochondria-dependent apoptosis signaling pathways via the activation of caspase-3 and PARP induced by Arctigenin. Cleaved caspase-8 and cleaved caspase-9 induced the activation of caspase-3 and PARP in FaDu cells treated with Arctigenin.
Korean J Physiol Pharmacol 2022;26:447-456 https://doi.org/10.4196/kjpp.2022.26.6.447
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