Customer Publication

AMG232 inhibits the angiogenesis in glioma through p53/RBM4/VEGFR2 pathway

Authors: Xiao, Yao et al.

Journal: Journal of Cell Science (2023)

Institution: Department of Neurobiology, School of Life Sciences, China Medical University, Shenyang, People's Republic of China

Research Areas: Cancer Research

Cell Lines: hCMEC/D3, U87, SVG12 (human cerebral microvascular endothelial cell line, human glioma cells, human astrocytes)

Summary: AMG232 effectively inhibits cancers with wild-type p53 by reactivating p53, but whether it inhibits glioma angiogenesis remains unclear. This study confirmed AMG232 inhibited the proliferation of glioma endothelial cells (GECs) in a dose-dependent manner and inhibited the angiogenesis of GECs, this finding providing a new target for the diagnosis and therapy of glioma. The study showed that AMG232 up-regulated the expression of p53 by blocking the MDM2-p53 interaction and in turn, promoted the expression of RBM4 in GECs, which targeted bound to VEGFR2 to promote its degradation, thereby inhibiting glioma angiogenesis. HoloMonitor was used to observe the effect of AMG232 on the migration of glioma endothelial cells (GECs).

Keywords: HoloMonitor M4, cell migration assay, single cell tracking, AMG232, p53, RBM4, VEGFR2, glioma, angiogenesis.

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