Evidence map›Paper›PMID 32606775›Full record

ArticleOncoTargets and therapy2020

Eicosapentaenoic acid's metabolism of 15-LOX-1 promotes the expression of miR-101 thus inhibits Cox2 pathway in colon cancer.

Yi Cai, Jie Liu, Shao-Kang Cai, Er-Ya Miao, Cheng-Qian Jia, Yong-Zhi Fan, Ying-Bo Li

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.5field-weighted citation impact, top 44% 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

8 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. T-Cadherin (International journal of molecular sciences · 2025
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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

7 authors at 1 institution in 1 country.

Yi Cai *Department of Pain Management, The Center Hospital of Wuhan, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei, People's Republic of China.
Jie Liu *Department of Pathology, The Center Hospital of Wuhan, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei, People's Republic of China.
Shao-Kang CaiDepartment of Pain Management, The Center Hospital of Wuhan, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei, People's Republic of China.
Er-Ya MiaoDepartment of Pain Management, The Center Hospital of Wuhan, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei, People's Republic of China.
Cheng-Qian JiaDepartment of Pain Management, The Center Hospital of Wuhan, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei, People's Republic of China.
Yong-Zhi FanDepartment of Pain Management, The Center Hospital of Wuhan, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei, People's Republic of China.
Ying-Bo LiDepartment of Pain Management, The Center Hospital of Wuhan, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei, People's Republic of China.
Huazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeIt is well known that diet Eicosapentaenoic acid (EPA) is beneficial to colon cancer (CC). However,  the underlying molecular mechanisms of EPA-relating miRNAs on genesis and development of this area is still unclear. MATERIALS AND

methodsThis study tries to find the function and specific role of EPA in CC through quantitative PCR (qPCR), Western blotting, immunofluorescence (IF), mass spectrometry, and immunohistochemistry (IHC) assays. By these methods, the enrichment of 15-LOX-1 metabolites of EPA, the expression of miR-101 and Cox2, and the relationship among them in CC are measured.

resultsThe quantity of miR-101 was obviously suppressed in CC tissues and SW480 cells. After application of miR-101 mimics in CC cell lines, the Cox2 expression was inhibited too. Next, we confirmed that EPA could increase the expression of miR-101 induced by 15-LOX-1. Finally, we tested whether EPA functions as a regulator of miR-101 via the production of resolvin E3.

conclusionOur data demonstrate that the EPA-15-LOX-1-miR-101-Cox2 signaling pathway owns a crucial position in the pathogenesis and development of diet-related CC. These findings exert exciting meanings for presenting new therapeutic angles in CC.

Indexed as

15-LOX-1colon cancerCox2EPAmiR-101

Identifiers

PMID32606775
PMCPMC7305347
OpenAlexW3035042711

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.