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. Author manuscript; available in PMC: 2017 Nov 14.
Published in final edited form as: Cancer Cell. 2016 Nov 14;30(5):723–736. doi: 10.1016/j.ccell.2016.10.001

Figure 7. XPO5 Phosphorylation by ERK Leads to Taxol Resistance in Liver Cancer by Decreasing miR-122 Export.

Figure 7

Under basal condition, pre-miR-122 is exported by XPO5 to produce mature miR-122 to inhibit SEPT9 expression. Un-phosphorylated MAP4 binds to tubulin to maintain taxol sensitivity. When ERK is activated, XPO5 is phosphorylated followed by isomerization by Pin1, which impairs its ability to load pre-miR-122. SEPT9 then acts as a scaffold for MAP4 and MARK4 to cause phosphorylated MAP4 to detach from microtubules therefore conferring taxol resistance.