Evidence map›Paper›PMID 29018241›Full record

ArticleScientific reports2017

Eugenol inhibits oxidative phosphorylation and fatty acid oxidation via downregulation of c-Myc/PGC-1β/ERRα signaling pathway in MCF10A-ras cells.

Xianxin Yan, Guijuan Zhang, Fengjie Bie, Yanhong Lv, Yi Ma, Min Ma, Yurong Wang, Xiaoqian Hao, Naijun Yuan, Xuefeng Jiang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

21 citing papers in PubMed, 38 citations in OpenAlex.

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  12. Lipid metabolism and cancer.The Journal of experimental medicine · 2021
    Review
  13. Pleiotropic Effects of Eugenol: The Good, the Bad, and the Unknown.Oxidative medicine and cellular longevity · 2021
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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

10 authors at 2 institutions in 1 country.

Xianxin YanCollege of Traditional Chinese Medicine, Jinan University, Guangzhou, China.
Guijuan ZhangThe School Outpatient Department, the First Affiliated Hospital of Jinan University, Guangzhou, China.
Fengjie BieCollege of Traditional Chinese Medicine, Jinan University, Guangzhou, China.
Yanhong LvCollege of Traditional Chinese Medicine, Jinan University, Guangzhou, China.
Yi MaBio-engineering institute of Jinan University, Guangzhou, China.
Min MaCollege of Traditional Chinese Medicine, Jinan University, Guangzhou, China. tmamin@jnu.edu.cn.
Yurong WangCollege of Traditional Chinese Medicine, Jinan University, Guangzhou, China.
Xiaoqian HaoCollege of Traditional Chinese Medicine, Jinan University, Guangzhou, China.
Naijun YuanCollege of Traditional Chinese Medicine, Jinan University, Guangzhou, China.
Xuefeng JiangCollege of Traditional Chinese Medicine, Jinan University, Guangzhou, China.
Jinan University · CNFirst Affiliated Hospital of Jinan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alteration in cellular energy metabolism plays a critical role in the development and progression of cancer. Targeting metabolic pathways for cancer treatment has been investigated as potential preventive or therapeutic methods. Eugenol (Eu), a major volatile constituent of clove essential oil mainly obtained from Syzygium, has been reported as a potential chemopreventive drug. However, the mechanism by which Eu regulates cellular energy metabolism is still not well defined. This study was designed to determine the effect of Eu on cellular energy metabolism during early cancer progression employing untransformed and H-ras oncogene transfected MCF10A human breast epithelial cells. Eu showed dose-dependent selective cytotoxicity toward MCF10A-ras cells but exhibited no apparent cytotoxicity in MCF10A cells. Treatment with Eu also significantly reduced intracellular ATP levels in MCF10A-ras cells but not in MCF10A cells. This effect was mediated mainly through inhibiting oxidative phosphorylation (OXPHOS) complexs and the expression of fatty acid oxidation (FAO) proteins including PPARα, MCAD and CPT1C by downregulating c-Myc/PGC-1β/ERRα pathway and decreasing oxidative stress in MCF10A-ras cells. These results indicate a novel mechanism involving the regulation of cellular energy metabolism by which Eu may prevent breast cancer progression.

Indexed as

Adenosine TriphosphateCarrier ProteinsCell Line, TumorCell SurvivalDown-RegulationERRalpha Estrogen-Related ReceptorEugenolFatty AcidsHumansModels, BiologicalOxidation-ReductionOxidative PhosphorylationOxidative StressProto-Oncogene Proteins c-mycras ProteinsReceptors, EstrogenAdenosine TriphosphateCarrier ProteinsERRalpha Estrogen-Related ReceptorEugenolFatty AcidsPPARGC1B protein, humanProto-Oncogene Proteins c-mycras ProteinsReceptors, EstrogenRNA-Binding Proteins

Identifiers

PMID29018241
PMCPMC5634997
OpenAlexW2763861766

What OpenQuestion holds

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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.