Fig. 8: Mechanism of CD5L-induced AVA resistance.
From: Overcoming adaptive resistance to anti-VEGF therapy by targeting CD5L
Anti-VEGF treatment may initially cause tumor regression via decreased angiogenesis (tumor with low vessel density); however, adaptive resistance frequently emerges over time, leading to tumor growth and increased angiogenesis (larger tumor with high vessel density). Inset demonstrates tumor endothelial cells showing that local tumor hypoxia leads to increased CD5L secretion by overexpression of transcription factor PPARG. Secreted CD5L binds to the CD36 receptor, causing activation of the AKT pathway and ultimately leading to increased cell proliferation and angiogenesis.
