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. 2016 May 10;7(25):37693–37713. doi: 10.18632/oncotarget.9264

Figure 12. Proposed model underlying the mechanism of entinostat potentiation of paclitaxel-mediated antitumor activity against NSCLC.

Figure 12

Entinostat enhances expression of miR-203 (in vitro and in vivo) and miR-542-3p (in vitro) via inhibition of HDAC, downregulation of DNMT1, and/or other mechanisms to reduce Survivin, and thereby potentiate paclitaxel-induced apoptosis in NSCLC cells. The combinations of entinostat and paclitaxel exert potent antitumor activity against NSCLC likely due to dramatic reduction of DNMT1 through an unknown mechanism to release promoter methylation-mediated epigenetic silencing of miR-203.