Skip to main content
. 2015 Sep 30;6(34):35183–35201. doi: 10.18632/oncotarget.5930

Figure 7. Schematic representation of the proposed molecular mechanism.

Figure 7

In highly metastatic lung cancer cells miR-145-5p expression is maintained at low levels by epigenetic modifications, such as hypermetylation and deacetylation of its promoter. Treatments with epigenetic drugs, such as vorinostat (SAHA) and 5-azacytidine (5-aza), could restore miR-145-5p expression, that in turns has a strong inhibitory effect on OCT-4, EGFR, MUC-1, MYC and TPD52 proteins expression. In particular MUC1 protein down-regulation potentiates the inhibitory effect on EGFR activity as it prevents EGFR nuclear localization. The final effect of miR-145-5p multi-targeting activity restoration results in a significant inhibition of the migratory ability of lung cancer.