Apatinib curbs TNBC vesicle-driven angiogenesis by lowering CRKII
- Label-free proteomics of triple-negative breast cancer small extracellular vesicles flagged the adaptor protein CRKII as a hub that apatinib pushes down.
- Less vesicle CRKII weakened pro-angiogenic signaling to endothelial cells via the PXN/VEGFA axis; CRKII knockdown mimicked the drug and overexpression reversed it.
- In a syngeneic mouse model, apatinib slowed tumor growth and lowered microvessel density, hinting at adjuvant value against recurrence.
💡 Points
Lower vesicle CRKII could be a mechanism of apatinib or just a downstream readout of VEGFR2 blockade. Knockdown and rescue make the link convincing in cells, but it has to hold at clinically reachable exposure. And slower growth with fewer vessels in a syngeneic model says little about recurrence yet; the adjuvant idea remains a hypothesis.