ArticleCancer science2026
EPHX2 Loss Promotes CRC Migration via EET-Dependent Chemokine Elevation and Mitochondrial Defect.
Article in Cancer science, 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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11 authors.
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Abstract
Epoxide hydrolase 2 (EPHX2) is a key enzyme in fatty acid metabolism that metabolizes epoxyeicosatrienoic acids (EETs), lipid mediators involved in inflammation, angiogenesis, and carcinogenesis. However, the role and mechanism of EPHX2 in colorectal cancer (CRC) migration remain unclear. In this study, we employed an integrated approach of bioinformatics and functional experiments to examine EPHX2 expression, its clinical implications, and its mechanistic role in CRC migration. Our results showed that EPHX2 was significantly downregulated in CRC tissues, and its low expression correlated with poor prognosis. Overexpression of EPHX2 led to accumulation of HDHA, HEPE, and HETE in CRC cells, whereas loss of EPHX2 increased CXCL levels and suppressed mitochondrial biogenesis via EET accumulation. Furthermore, loss of EPHX2 promoted cell migration through ROS and CXCL signaling. Collectively, loss of EPHX2 accelerates cell migration via EET accumulation-dependent chemokine elevation and mitochondrial biogenesis impairment in CRC. These findings reveal a novel metabolic-mitochondrial axis in CRC progression and highlight EPHX2 as a potential therapeutic target.
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