Evidence map›Paper›PMID 30519106›Full record

ArticleCancer management and research2018

Tumor-suppressive function of SIRT4 in neuroblastoma through mitochondrial damage.

Yumei Wang, Yinmou Guo, Jianzhi Gao, Xiangdong Yuan

Abstract read
In one paragraph

Article in Cancer management and research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Research Progress of Sirtuin4 in Cancer.Frontiers in oncology · 2020
    Review
  12. The sirtuin family in cancer.Cell cycle (Georgetown, Tex.) · 2019
    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

4 authors.

Yumei WangDepartment of Children's Rehabilitation, Shangqiu First People's Hospital of Henan, Shangqiu, Henan, China.
Yinmou GuoFirst Department of Oncology, Shangqiu First People's Hospital of Henan, Shangqiu, Henan, China, guoym59@163.com.
Jianzhi GaoDepartment of Oncology, Zhuozhou Hospital of Beijing 301 Hospital, Beijing, China.
Xiangdong YuanDepartment of Children's Rehabilitation, Shangqiu First People's Hospital of Henan, Shangqiu, Henan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSIRT4 is a member of the sirtuin family of nicotinamide adenine dinucleotide-dependent enzymes located in the mitochondria, and is involved in regulating energy metabolism, stress response, and cellular lifespan in mammalian cells. However, its function in human neuroblastoma (NB) remains unexplored.

methodsExpression of SIRT4 in 158 pairs of human NB tumor tissues and adjacent normal tissues collected from March 2009 to October 2012 was analyzed by immunohistochemistry, Western blotting, and real-time fluorescence quantitative PCR. For in vitro study, SIRT4 was overexpressed in SH-SY5Y, SK-N-BE, and IMR-32 cells to study the effects of SIRT4 expression on proliferation, invasion, and migration of human NB cells and on mitochondrial function.

resultsSIRT4 gene expression in human NB tumor tissues was significantly lower than that in adjacent normal tissues (

conclusionSIRT4 exhibits a tumor suppressor function in human NB and inhibits mitochondrial metabolism and SIRT1 expression in tumor cells, thereby reducing the energy metabolism of tumor cells. These results suggest that SIRT4 may be a new therapeutic target for human NB.

Indexed as

energy metabolismneuroblastomaSIRT1SIRT4

Identifiers

PMID30519106
PMCPMC6234993

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.