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Arachidonic acid metabolism as a novel pathogenic factor in gastrointestinal cancers.

作者信息

Lu Weiqin, Aihaiti Aihemaitijiang, Abudukeranmu Paziliya, Liu Yajun, Gao Huihui

机构信息

General Surgery, Cancer Center, Department of Vascular Surgery, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, China.

Aksu First People's Hospital, Xinjiang, China.

出版信息

Mol Cell Biochem. 2025 Feb;480(2):1225-1239. doi: 10.1007/s11010-024-05057-2. Epub 2024 Jul 4.


DOI:10.1007/s11010-024-05057-2
PMID:38963615
Abstract

Gastrointestinal (GI) cancers are a major global health burden, representing 20% of all cancer diagnoses and 22.5% of global cancer-related deaths. Their aggressive nature and resistance to treatment pose a significant challenge, with late-stage survival rates below 15% at five years. Therefore, there is an urgent need to delve deeper into the mechanisms of gastrointestinal cancer progression and optimize treatment strategies. Increasing evidence highlights the active involvement of abnormal arachidonic acid (AA) metabolism in various cancers. AA is a fatty acid mainly metabolized into diverse bioactive compounds by three enzymes: cyclooxygenase, lipoxygenase, and cytochrome P450 enzymes. Abnormal AA metabolism and altered levels of its metabolites may play a pivotal role in the development of GI cancers. However, the underlying mechanisms remain unclear. This review highlights a unique perspective by focusing on the abnormal metabolism of AA and its involvement in GI cancers. We summarize the latest advancements in understanding AA metabolism in GI cancers, outlining changes in AA levels and their potential role in liver, colorectal, pancreatic, esophageal, gastric, and gallbladder cancers. Moreover, we also explore the potential of targeting abnormal AA metabolism for future therapies, considering the current need to explore AA metabolism in GI cancers and outlining promising avenues for further research. Ultimately, such investigations aim to improve treatment options for patients with GI cancers and pave the way for better cancer management in this area.

摘要

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[2]
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本文引用的文献

[1]
Carrier-free self-assembled nanomedicine based on celastrol and galactose for targeting therapy of hepatocellular carcinoma via inducing ferroptosis.

Eur J Med Chem. 2024-3-5

[2]
Dual COX-2/5-LOX inhibitors from inhibit gastric cancer cells by cross-mediating thyroid, estrogen, and oxytocin signaling pathways.

Front Chem. 2024-1-10

[3]
Arenobufagin regulates the p62-Keap1-Nrf2 pathway to induce autophagy-dependent ferroptosis in HepG2 cells.

Naunyn Schmiedebergs Arch Pharmacol. 2024-7

[4]
From synergy to resistance: Navigating the complex relationship between sorafenib and ferroptosis in hepatocellular carcinoma.

Biomed Pharmacother. 2024-1

[5]
Inhibiting cholesterol de novo synthesis promotes hepatocellular carcinoma progression by upregulating prostaglandin E synthase 2-mediated arachidonic acid metabolism under high fatty acid conditions.

Cancer Sci. 2024-2

[6]
Oncogenic PIK3CA recruits myeloid-derived suppressor cells to shape the immunosuppressive tumour microenvironment in luminal breast cancer through the 5-lipoxygenase-dependent arachidonic acid pathway.

Clin Transl Med. 2023-11

[7]
Arachidonic acid metabolism CYP450 pathway is deregulated in hepatocellular carcinoma and associated with microvascular invasion.

Cell Biol Int. 2024-1

[8]
ENO1 promotes liver carcinogenesis through YAP1-dependent arachidonic acid metabolism.

Nat Chem Biol. 2023-12

[9]
Regulation of inflammation in cancer by dietary eicosanoids.

Pharmacol Ther. 2023-8

[10]
Patient-derived models facilitate precision medicine in liver cancer by remodeling cell-matrix interaction.

Front Immunol. 2023

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