Evidence map›Paper›PMID 30972978›Full record

ArticleCancer medicine2019

Zinc cooperates with p53 to inhibit the activity of mitochondrial aconitase through reactive oxygen species accumulation.

Ya-Nan Xue, Ya-Nan Liu, Jing Su, Jiu-Ling Li, Yao Wu, Rui Guo, Bing-Bing Yu, Xiao-Yu Yan, Li-Chao Zhang, Lian-Kun Sun and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2019. 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
1.1field-weighted citation impact, top 26% 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, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Cuproptosis: p53-regulated metabolic cell death?Cell death and differentiation · 2023
    Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  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

11 authors at 1 institution in 1 country.

Ya-Nan XueDepartment of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin, China.ORCID 0000-0002-4015-2709
Ya-Nan LiuDepartment of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin, China.
Jing SuDepartment of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin, China.
Jiu-Ling LiDepartment of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin, China.
Yao WuDepartment of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin, China.
Rui GuoDepartment of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin, China.
Bing-Bing YuDepartment of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin, China.
Xiao-Yu YanDepartment of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin, China.ORCID 0000-0002-6417-8380
Li-Chao ZhangDepartment of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin, China.
Lian-Kun SunDepartment of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin, China.
Yang LiDepartment of Pathophysiology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin, China.
Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic reprogramming is a central hallmark of cancer. Therefore, targeting metabolism may provide an effective strategy for identifying promising drug targets for cancer treatment. In prostate cancer, cells undergo metabolic transformation from zinc-accumulating, citrate-producing cells to citrate-oxidizing malignant cells with lower zinc levels and higher mitochondrial aconitase (ACO2) activity. ACO2 is a Krebs cycle enzyme that converts citrate to isocitrate and is sensitive to reactive oxygen species (ROS)-mediated damage. In this study, we found that the expression of ACO2 is positively correlated with the malignancy of prostate cancer. Both zinc and p53 can lead to an increase in ROS. ACO2 can be a target for remodeling metabolism by sensing changes in the ROS levels of prostate cancer. Our results indicate that targeting ACO2 through zinc and p53 can change prostate cancer metabolism, and thus provides a potential new therapeutic strategy for prostate cancer.

Indexed as

Aconitate HydrataseAnimalsCell Line, TumorDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansMaleMicePaclitaxelPC-3 CellsProstatic NeoplasmsReactive Oxygen SpeciesTumor Suppressor Protein p53Up-RegulationXenograft Model Antitumor AssaysZincACO2 protein, humanAconitate HydratasePaclitaxelReactive Oxygen SpeciesTumor Suppressor Protein p53Zincmitochondrial aconitasep53ROSzinc

Identifiers

PMID30972978
PMCPMC6536939
OpenAlexW2935914586

What OpenQuestion 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 OpenQuestion graph.