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. 2015 Apr 15;6(18):16396–16410. doi: 10.18632/oncotarget.3844

Figure 7. Schematic representation of the crosstalk between HNK and Stat3-miR-34a and Wnt1-MTA1-β-catenin axes.

Figure 7

Leptin treatment induces phosphorylation of Stat3 leading to increased recruitment of Stat3 to miR34a resulting in repression of miR34a. Inhibition of miR34a allows increased levels of Wnt1 expression in the presence of leptin. Leptin treatment results in stabilization and nuclear localization of βcatenin increasing activation of Wnt/βcatenin responsive genes. Honokiol treatment inhibits leptin-induced phosphorylation of Stat3, releases Stat3 from the conserved Stat3-binding site located in the first intron of miR-34a hence releasing the repressive effects of Stat3 and increasing miR34a expression. miR34a represses Wnt1 expression. Honokiol treatment results in abrogation of Wnt/βcatenin signaling pathway even in the presence of leptin.