An Ovol1 Variant in Endothelial Cells Regulates Slug and is Essential for Pathological Angiogenesis

An endothelial Ovol1 low molecular weight variant directly binds the Slug gene and upregulates Slug, driving pEndoMT and hypersprouting in endothelial cells.

• Why it matters: Pathological angiogenesis involves dysregulated sprouting and excessive, disorganized vessels, but upstream signals that activate Slug and pEndoMT in disease remain unclear.
• What they did: They used ChIP to confirm Ovol1 binding to the endogenous Slug locus, then applied Ovol1 silencing and lentiviral overexpression in endothelial cells to measure pEndoMT markers and migration, plus 3D sprouting assays.
• The result: Ovol1 knockdown abolished 3D sprouting angiogenesis, while Ovol1 overexpression caused overaggressive, disorganized hypersprouting dependent on Slug; in mice, Ovol1ECKO and SlugECKO reduced colorectal cancer syngraft growth and tumor angiogenesis and reduced neovascularization in OIR.

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