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. 2018 Jan 10;10(1):14. doi: 10.3390/cancers10010014

Figure 2.

Figure 2

Targeting de novo mesenchymal/cancer stem cell (Mes/CSC) plasticity. Epithelial/non-cancer stem cells acquire mutations within oncogenes or are exposed to extrinsic factors capable of driving them to a mesenchymal/CSC (Mes/CSC) state. This Mes/CSC plasticity imparts increased migration and metastases, tumor initiation, and importantly therapeutic resistance. In order to combat this cell plasticity, one can utilize neutralizing antibodies targeting extrinsic drivers (i.e., Oncostatin M (OSM), Transforming Growth Factor-β (TGF-β), Tumor Necrosis Factor-α (TNF-α)), and blocking peptides or small molecules targeted toward intrinsic drivers (i.e., Family with Sequence Similarity 83 Member A (FAM83A), KRAS, PI3K) of cell plasticity to prevent Mes/CSC induction or revert the Mes/CSC state into a more drug sensitive epithelial/non-CSC state. TME: tumor microenvironment.