The lipid-metabolism enzyme ECI2 reduces neutrophil extracellular traps formation for colorectal cancer suppression

Lixia Chen, Peiling Dai, Lei Liu, Yujia Chen, Yanxia Lu, Lin Zheng, Haowei Wang, Qinzi Yuan and Xuenong Li ()
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Lixia Chen: Southern Medical University
Peiling Dai: Southern Medical University
Lei Liu: Southern Medical University
Yujia Chen: Southern Medical University
Yanxia Lu: Southern Medical University
Lin Zheng: Southern Medical University
Haowei Wang: Southern Medical University
Qinzi Yuan: Southern Medical University
Xuenong Li: Southern Medical University

Nature Communications, 2024, vol. 15, issue 1, 1-17

Abstract: Abstract Abnormalities in ether lipid metabolism as well as the formation of neutrophil extracellular traps have recently been recognized as detrimental factors affecting tumorigenesis and progression. However, the role of abnormal ether lipid metabolism in colorectal cancer (CRC) evolution has not been reported. Here we show that the lipid metabolism-related gene enoyl-CoA δ-isomerase 2 (ECI2) plays a tumor-suppressor role in CRC and is negatively associated with poor prognosis in CRC patients. We mechanistically demonstrate that ECI2 reduces ether lipid-mediated Interleukin 8 (IL-8) expression leading to decreased neutrophil recruitment and neutrophil extracellular traps formation for colorectal cancer suppression. In particular, ECI2 inhibits ether lipid production in CRC cells by inhibiting the peroxisomal localization of alkylglycerone phosphate synthase (AGPS), the rate-limiting enzyme for ether lipid synthesis. These findings not only deepen our understanding of the role of metabolic reprogramming and neutrophil interactions in the progression of CRC, but also provide ideas for identifying potential diagnostic markers and therapeutic targets for CRC.

Date: 2024
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DOI: 10.1038/s41467-024-51489-1

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