What question did this study set out to answer?

To investigate the role of 14,15-eicosatrienoic acid in intestinal adenoma growth and its potential as a biomarker for colorectal cancer.

March 14, 2026Open Access

14,15-epoxyeicosatrienoic acid drives intestinal adenoma growth and its value as an early biomarker for intestinal adenoma occurrence

Key Points

To investigate the role of 14,15-eicosatrienoic acid in intestinal adenoma growth and its potential as a biomarker for colorectal cancer.
Utilized targeted metabolomics with ultra performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS)
Analyzed serum levels of 14,15-EET in ApcMin/+ adenoma model mice and C57BL/6 controls
Conducted ELISA and bioinformatics analyses on adenoma and CRC patients
Conducted functional studies to assess 14,15-EET's effects on adenoma growth and cellular behaviors
Elevated serum 14,15-EET levels detected in ApcMin/+ mice prior to adenoma onset
Similar elevation in patients with adenomas and CRC
In vivo studies showed 14,15-EET accelerated adenoma growth
In vitro studies demonstrated increased proliferation, migration, and invasion linked to AKT/ERK1/2 signaling activation

Abstract

Intestinal adenomas are premalignant lesions that develop into colorectal cancer (CRC), yet the metabolic pathways underlying their malignant transformation remain poorly characterized. Using targeted metabolomics via ultra performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS), we found that serum levels of the bioactive lipid metabolite 14,15-epoxyeicosatrienoic acid (14,15-EET) were dramatically elevated in ApcMin/+ adenoma model mice as early as pre-adenoma stages, compared to C57BL/6 controls. The results were also consistent in adenomas and CRC patients. ELISA data and bioinformatics analyses revealed both elevated serum 14,15-EET levels and upregulated cytochrome P450 2J2 (CYP2J2) expression in tumor. Functional studies showed that 14,15-EET accelerates adenoma growth in vivo, and promotes proliferation, migration, and invasion in vitro by activating AKT (Ser473)/ERK1/2 signaling and inducing epithelial-mesenchymal transition (EMT). Its early elevation in premalignant lesions, and relative molecules 14,15-EET/CYP2J2 represents a novel strategy for disrupting adenoma-carcinoma transition, and offering new biomarker for CRC prevention.

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