ArticleCell death & disease2026
Proteolytic EphA2 fragments cooperatively promote hepatocellular carcinoma progression.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
EphA2 is a receptor tyrosine kinase that suppresses tumor growth when bound by its ligand ephrin-A1 (EA1), but promotes tumor progression in the absence of ligand. In hepatocellular carcinoma (HCC) cells, EphA2 is proteolytically cleaved by membrane-type 1 matrix metalloproteinase (MT1-MMP), producing a C-terminal fragment (EphA2-CF) and an N-terminal fragment (EphA2-NF). The functional role of these cleavage fragments on HCC remains unclear. Herein, we investigated their roles in hepatocarcinogenesis and malignant progression. Western blotting and membrane biotinylation assays revealed that EphA2-CF was present in HCC cells co-expressing EphA2 and MT1-MMP. EphA2-CF-expressing cells were resistant to EA1-induced growth suppression, while MT1-MMP knockdown restored EA1 sensitivity. In Hep3B cells, stable EphA2-CF expression confirmed resistance to EA1-mediated inhibition of proliferation and survival. Mechanistically, EphA2-CF sustained oncogenic signaling through constitutive phosphorylation at EphA2-S
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