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. 2017 Dec 19;9(2):2931–2950. doi: 10.18632/oncotarget.23407

Figure 2. Schematic Diagram of Reactive Oxygen Species (ROS)-Related Anticancer Effects Mediated by Ginsenosides.

Figure 2

Up-regulation: Fas, Bid, tBid, Bax, Bad, p53, p21, p27, p16, caspase-3, caspase-8, caspase-9, ER (endoplasmic reticulum) stress, DR5, CHOP, ATF-6, Smac, PERK, HO-1, EGFR, Beclin 1, Atg7, Atg5, LC3-I, LC3-II, AMP-activated protein kinase (AMPK), MEK signaling pathway, ASK-1/JNK signaling pathway, estrogen receptor 2 (ESR2)-neutrophil cytosolic factor 1 (NCF1)-ROS signaling pathway, ER (estrogen receptor)-dependent PI3K/Akt/ Nrf2 pathway, P53-CHOP pathways, and ROS–JNK–autophagy pathways. Down-regulation: Ki-67, cyclinD1, cyclin E, CDK2/4, cdc25, cyclin B1, survivin, cFLIP, Mcl-1, XIAP, Bcl-2, cytosol Cat B, cytosolic vacuolization, CD34, VEGF, COX-2, PGE2, MMP-9 and PI3K/Akt signaling pathway.