Evidence map›Paper›PMID 27374097›Full record

ArticleOncotarget2016

Metabolomics profiles delineate uridine deficiency contributes to mitochondria-mediated apoptosis induced by celastrol in human acute promyelocytic leukemia cells.

Xiaoling Zhang, Jing Yang, Minjian Chen, Lei Li, Fei Huan, Aiping Li, Yanqing Liu, Yankai Xia, Jin-Ao Duan, Shiping Ma

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
7.1field-weighted citation impact, top 4% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

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  14. Spatially resolved metabolomics to discover tumor-associated metabolic alterations.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  15. Article
  16. Application of Metabolomics in the Study of Natural Products.Natural products and bioprospecting · 2018
    Article
  17. Review
  18. Article
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 3 institutions in 1 country.

Xiaoling ZhangDepartment of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing 210009, China.
Jing YangDepartment of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing 210009, China.
Minjian ChenState Key Laboratory of Reproductive Medicine, Institute of Toxicology, Nanjing Medical University, Nanjing 211166, China.
Lei LiDepartment of Hygienic Analysis and Detection, Nanjing Medical University, Nanjing 211166, China.
Fei HuanSafety Assessment and Research Center for Drug, Pesticide and Veterinary Drug of Jiangsu Province, Nanjing Medical University, Nanjing 211166, China.
Aiping LiKey Laboratory of Modern Toxicology of Ministry of Education, Nanjing Medical University, Nanjing 211166, China.
Yanqing LiuKey Laboratory of Modern Toxicology of Ministry of Education, Nanjing Medical University, Nanjing 211166, China.
Yankai XiaState Key Laboratory of Reproductive Medicine, Institute of Toxicology, Nanjing Medical University, Nanjing 211166, China.
Jin-Ao DuanNational and Local Collaborative Engineering Center of Chinese Medicinal Resources Industrialization and Formulae Innovative Medicine, Nanjing University of Chinese Medicine, Nanjing 210023, China.
Shiping MaDepartment of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing 210009, China.
Nanjing Medical University · CNChina Pharmaceutical University · CNNanjing University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Celastrol, extracted from "Thunder of God Vine", is a promising anti-cancer natural product. However, its effect on acute promyelocytic leukemia (APL) and underlying molecular mechanism are poorly understood. The purpose of this study was to explore its effect on APL and underlying mechanism based on metabolomics. Firstly, multiple assays indicated that celastrol could induce apoptosis of APL cells via p53-activated mitochondrial pathway. Secondly, unbiased metabolomics revealed that uridine was the most notable changed metabolite. Further study verified that uridine could reverse the apoptosis induced by celastrol. The decreased uridine was caused by suppressing the expression of gene encoding Dihydroorotate dehydrogenase, whose inhibitor could also induce apoptosis of APL cells. At last, mouse model confirmed that celastrol inhibited tumor growth through enhanced apoptosis. Celastrol could also decrease uridine and DHODH protein level in tumor tissues. Our in vivo study also indicated that celastrol had no systemic toxicity at pharmacological dose (2 mg/kg, i.p., 21 days). Altogether, our metabolomics study firstly reveals that uridine deficiency contributes to mitochondrial apoptosis induced by celastrol in APL cells. Celastrol shows great potential for the treatment of APL.

Indexed as

MetabolomicsAnimalsApoptosisDihydroorotate DehydrogenaseHL-60 CellsHumansLeukemia, Promyelocytic, AcuteMiceMitochondriaOxidoreductases Acting on CH-CH Group DonorsPentacyclic TriterpenesTriterpenesTumor Suppressor Protein p53UridineXenograft Model Antitumor AssayscelastrolDihydroorotate DehydrogenaseOxidoreductases Acting on CH-CH Group DonorsPentacyclic TriterpenesTriterpenesTumor Suppressor Protein p53Uridineacute promyelocytic leukemiaapoptosiscelastrolmetabolomicsuridine

Identifiers

PMID27374097
PMCPMC5216817
OpenAlexW2472864907

What OpenQuestion holds

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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 OpenQuestion graph.