Evidence map›Paper›PMID 21030485›Full record

ArticleThe Journal of pharmacology and experimental therapeutics2011

Cytochrome P450 2J2 is highly expressed in hematologic malignant diseases and promotes tumor cell growth.

Chen Chen, Xin Wei, Xiaoquan Rao, Jun Wu, Shenglan Yang, Fuqiong Chen, Ding Ma, Jianfeng Zhou, Ryan T Dackor, Darryl C Zeldin and 1 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of pharmacology and experimental therapeutics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
4.5field-weighted citation impact, top 5% of its field
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

46 citing papers in PubMed, 101 citations in OpenAlex.

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  14. Soluble epoxide hydrolase (Archives of medical science : AMS · 2021
    Article
  15. Cyp2c44 regulates prostaglandin synthesis, lymphangiogenesis, and metastasis in a mouse model of breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
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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

11 authors at 3 institutions in 2 countries.

Chen ChenDepartment of Internal Medicine and Gene Therapy Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China.
Xin Wei
Xiaoquan Rao
Jun Wu
Shenglan Yang
Fuqiong Chen
Ding Ma
Jianfeng Zhou
Ryan T Dackor
Darryl C Zeldin
Dao Wen Wang
Huazhong University of Science and Technology · CNNational Institutes of Health · USTongji Hospital · CN

Funding

Characterization And Functional Significance Of P450 Arachidonate EpoxygenasesZIAES025034 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI ZELDIN, DARRYL C · 2009 to 2025
$18.6M
P450 Arachidonate EpoxygenasesZ01ES025034 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI ZELDIN, DARRYL C · 1995 to 2008
$2.2M
Intramural NIH HHS Z01 ES025034NIEHS NIH HHS Z01-ES025034
6 · The paper itself

Abstract

Cytochrome P450 2J2 (CYP2J2) epoxygenase converts arachidonic acid to four regioisomeric epoxyeicosatrienoic acids (EETs) that exert multiple biological effects in the cardiovascular system and in various human solid cancers. However, it is unknown whether this enzyme is expressed or plays any role in malignant hematological diseases. In this study, we found strong and highly selective CYP2J2 expression in five human-derived malignant hematological cell lines and in leukemia cells from peripheral blood and bone marrow in 36 of 42 patients (86%) with malignant hematologic diseases. Furthermore, increased levels of EETs were detected in urine and blood samples from these patients. Addition of exogenous EET or CYP2J2 overexpression in cultured human-derived malignant hematologic cell lines markedly accelerated proliferation and attenuated apoptosis. Addition of the selective CYP2J2 inhibitor compound 26 (C26; 1-[4-(vinyl) phenyl]-4-[4-(diphenyl-hydroxymethyl)-piperidinyl]-butanone hydrochloride) inhibited cell proliferation and increased apoptosis, an effect that was significantly reversed by EET. CYP2J2 overexpression and exogenous EET activated AMP-activated protein kinase, c-Jun NH(2)-terminal kinase, and phosphatidylinositol 3-kinase/Akt signaling pathways, and increased epidermal growth factor receptor phosphorylation levels. CYP2J2 overexpression also enhanced malignant xenograft growth, which was efficiently inhibited by oral administration of C26 in Tie2-CYP2J2 transgenic mice and in severe combined immunodeficiency (SCID) xenograft mice. Together, these results suggest that CYP2J2 plays a key role in the pathogenesis of human hematologic malignant diseases. Selective inhibition of CYP2J2 may be a promising therapeutic strategy for these conditions.

Indexed as

AnimalsApoptosisCaspase 3Cell Line, TumorCell ProliferationCytochrome P-450 CYP2J2Cytochrome P-450 Enzyme InhibitorsCytochrome P-450 Enzyme SystemHumansLeukemiaMaleMiceMice, Inbred C57BLRNA, MessengerCaspase 3CYP2J2 protein, humanCytochrome P-450 CYP2J2Cytochrome P-450 Enzyme InhibitorsCytochrome P-450 Enzyme SystemRNA, Messenger

Identifiers

PMID21030485
PMCPMC3033713
OpenAlexW2125401061

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.