fig4
From: Drug resistance mechanisms of cancer stem-like cells and their therapeutic potential as drug targets
Figure 4. PI3K/Akt signaling pathway contributes to CSC maintenance and could be a promising target. When CD74-NRG1 fusion protein (in lung cancer) or heregulin (in breast cancer) binds to HER2/HER3 heterodimer receptor, PI3K/Akt/NF-κB signaling is activated. NF-κB induces gene expression of IGF-2 and growth differentiation factor 15 (GDF15), which enhances self-renewal ability of CSCs. Therefore, inhibition of this signaling pathway would be promising to target CSCs. IGF-2: insulin-like growth factor-2; GDF15: growth differentiation factor 15. CSCs: cancer stem-like cells
