Evidence mapPaperPMID 39695149Full record

ArticleCell death & disease2024

Epoxy metabolites of linoleic acid promote the development of breast cancer via orchestrating PLEC/NFκB1/CXCL9-mediated tumor growth and metastasis.

Kai-Di Ni, Xian Fu, Ying Luo, Xin He, Hou-Hua Yin, Dong-Ping Mo, Jing-Xian Wu, Ming-Jun Wu, Xiao Zheng, Ya-Nan Liu and 12 more

Abstract read
In one paragraph

Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed.

  1. Article
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  5. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

22 authors.

Kai-Di NiCNTTI of College of Pharmacy and Department of Anesthesia of the Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Xian FuCNTTI of College of Pharmacy and Department of Anesthesia of the Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Ying LuoDepartment of Clinical Laboratory, Shanghai Changning Maternity and Infant Health Hospital, East China Normal University, Shanghai, China.
Xin HeCNTTI of College of Pharmacy and Department of Anesthesia of the Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Hou-Hua YinCNTTI of College of Pharmacy and Department of Anesthesia of the Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Dong-Ping MoDepartment of Clinical Laboratory, Jiangsu Cancer Hospital, the Affiliated Cancer Hospital of Nanjing Medical University, Jiangsu Institute of Cancer Research, Nanjing, China.
Jing-Xian WuDepartment of Pathology, College of Basic Medicine of Chongqing Medical University, Chongqing, China.
Ming-Jun WuCenter for Science & technology Innovation, Chongqing Medical University, Chongqing, China.
Xiao ZhengBasic Medicine Research and Innovation Center for Novel Target and Therapeutic Intervention, Ministry of Education, Chongqing, China.
Ya-Nan LiuCNTTI of College of Pharmacy and Department of Anesthesia of the Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Qing JiangCNTTI of College of Pharmacy and Department of Anesthesia of the Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Ling-Tong ZhangCNTTI of College of Pharmacy and Department of Anesthesia of the Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Ai-Zhi LinCNTTI of College of Pharmacy and Department of Anesthesia of the Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Ling HuangCNTTI of College of Pharmacy and Department of Anesthesia of the Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Qing-Jin PanBasic Medicine Research and Innovation Center for Novel Target and Therapeutic Intervention, Ministry of Education, Chongqing, China.
Xue-Dong YinThe Department of Breast and Thyroid surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Huan-Yu ZhangThe Second Clinical College of Chongqing Medical University, Chongqing, China.
Yi-Wen MengCNTTI of College of Pharmacy and Department of Anesthesia of the Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Xue ZhouCNTTI of College of Pharmacy and Department of Anesthesia of the Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Jianbo PanBasic Medicine Research and Innovation Center for Novel Target and Therapeutic Intervention, Ministry of Education, Chongqing, China.ORCID 0000-0001-6014-8160
Zufeng GuoBasic Medicine Research and Innovation Center for Novel Target and Therapeutic Intervention, Ministry of Education, Chongqing, China.ORCID 0000-0002-4370-9445
Jun-Yan LiuCNTTI of College of Pharmacy and Department of Anesthesia of the Second Affiliated Hospital, Chongqing Medical University, Chongqing, China. jyliu@cqmu.edu.cn.ORCID 0000-0002-3018-0335

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82273408
6 · The paper itself

Abstract

Breast cancer (BC) is a common malignant tumor in women and requires a comprehensive understanding of its pathogenesis for the development of new therapeutic strategies. Polyunsaturated fatty acids (PUFAs) metabolism-driven inflammation is a causative factor in cancer development. However, the function of PUFAs' metabolism in BC remains largely unknown. Here we report the role and underlying mechanism of epoxyoctadecenoic acids (EpOMEs), the metabolites of linoleic acid mediated by cytochrome P450 (CYP) monooxygenases, in promoting the development of BC, particularly triple-negative BC (TNBC). A metabolomics study identified that EpOMEs were significantly increased in the plasma of BC patients and MMTV-PyMT mice, which accounted for the upregulation of CYP2J2 in BC tumor tissues and tumor cells. Decreased EpOMEs by treatment of CYP monooxygenase inhibitors significantly alleviated tumor development in MMTV-PyMT mice. Treatment with EpOMEs and overexpression of CYP2J2 to increase EpOMEs in TNBC cells significantly promoted cellular proliferation, migration, tumor growth, and metastasis. Whereas knockdown of CYP2J2 to decrease EpOMEs inhibited tumorigenesis and lung metastasis of TNBC, which was reversed by EpOME administration. Transcriptomics and proteomics analyses revealed CXCL9 and PLEC were critical for EpOME-mediated promotion of TNBC. Knockdown of CXCL9 and PLEC inhibited TNBC progression and EpOME-mediated promotion of TNBC. Both overexpression of CYP2J2 and EpOME treatment upregulate PLEC, while PLEC upregulates NFκB1, which is a transcription regulator of CXCL9. This study extends the understanding of the function of PUFAs metabolism in BC development, providing potential therapeutic targets and dietary guidelines for patients with TNBC and other BCs. The illustration of the hypothetical mechanism CYP2J2/EpOMEs promotes the tumorigenesis and metastasis of TNBC via PLEC/NFKB1/CXCL9 signaling pathway.

Indexed as

Cell ProliferationCytochrome P-450 CYP2J2Cytochrome P-450 Enzyme SystemLinoleic AcidAnimalsBreast NeoplasmsCell Line, TumorChemokine CXCL9FemaleHumansMiceNeoplasm MetastasisSignal TransductionTriple Negative Breast NeoplasmsChemokine CXCL9CYP2J2 protein, humanCytochrome P-450 CYP2J2Cytochrome P-450 Enzyme SystemLinoleic Acid

Identifiers

PMID39695149
PMCPMC11655665

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.