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Conversely, nicotine may exert paradoxical inhibitory effects by activating immune pathways and inducing apoptosis, such as through stimulation of immature dendritic cells via PI3K/Akt signaling and modulation of caspase-3 and Cyclin B1 expression through 7-nAChR signaling [36]

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c-MET signaling pathway [1] Beyond the classical HGF-dependent activation pathway, c-MET can also be activated through non-canonical pathways via interactions with other receptors such as integrin 64, EGFR, CD44v6, Plexin B, HER2, HER3, and AXL