Evidence map›Paper›PMID 29459713›Full record

ArticleOncogene2018

Elevated mitochondrial SLC25A29 in cancer modulates metabolic status by increasing mitochondria-derived nitric oxide.

Huiyuan Zhang, Qinyi Wang, Junzhong Gu, Le Yin, Shenghui Liang, Lida Wu, Hao Xu, Chao Zhao, Yuchun Gu

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.7field-weighted citation impact, top 36% 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

19 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
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

9 authors at 3 institutions in 2 countries.

Huiyuan ZhangLaboratory of Molecular Pharmacology, Institute of Molecular Medicine, Peking University, Beijing, China.
Qinyi WangLaboratory of Molecular Pharmacology, Institute of Molecular Medicine, Peking University, Beijing, China.
Junzhong GuLaboratory of Molecular Pharmacology, Institute of Molecular Medicine, Peking University, Beijing, China.
Le YinLaboratory of Molecular Pharmacology, Institute of Molecular Medicine, Peking University, Beijing, China.
Shenghui LiangLaboratory of Molecular Pharmacology, Institute of Molecular Medicine, Peking University, Beijing, China.
Lida WuLaboratory of Molecular Pharmacology, Institute of Molecular Medicine, Peking University, Beijing, China.
Hao XuLaboratory of Molecular Pharmacology, Institute of Molecular Medicine, Peking University, Beijing, China.
Chao ZhaoDepartment of Clinical Neurosciences, WT-MRC Cambridge Stem Cell Institute, Cambridge University, Cambridge, UK.
Yuchun GuLaboratory of Molecular Pharmacology, Institute of Molecular Medicine, Peking University, Beijing, China. ycgu@pku.edu.cn.
Peking University · CNAston University · GBUniversity of Cambridge · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Warburg effect has been recognized as a hallmark of cancer cells for many years, but its modulation mechanism remains a great focus. Our current study found a member of solute carrier family 25 (SLC25A29), the main arginine transporter on mitochondria, significantly elevated in various cancer cells. Knockout of SLC25A29 by CRISPR/Cas9 inhibited proliferation and migration of cancer cells both in vitro and in vivo. SLC25A29-knockout cells also showed an altered metabolic status with enhanced mitochondrial respiration and reduced glycolysis. All of above impacts could be reversed after rescuing SLC25A29 expression in SLC25A29-knockout cells. Arginine is transported into mitochondria partly for nitric oxide (NO) synthesis. Deletion of SLC25A29 resulted in severe decrease of NO production, indicating that the mitochondria is a significant source of NO. SLC25A29-knockout cells dramatically altered the variation of metabolic processes, whereas addition of arginine failed to reverse the effect, highlighting the necessity of transporting arginine into mitochondria by SLC25A29. In conclusion, aberrant elevated SLC25A29 in cancer functioned to transport more arginine into mitochondria, improved mitochondria-derived NO levels, thus modulated metabolic status to facilitate increased cancer progression.

Indexed as

Up-RegulationAnimalsArginineCarnitine AcyltransferasesDisease ProgressionGene Expression Regulation, NeoplasticGene Knockout TechniquesGlycolysisHeLa CellsHep G2 CellsHumansHuman Umbilical Vein Endothelial CellsMiceMitochondriaMitochondrial ProteinsNeoplasmsArginineCarnitine AcyltransferasesMitochondrial ProteinsNitric OxideSLC25A29 protein, human

Identifiers

PMID29459713
OpenAlexW2788442383

What OpenQuestion holds

Textmetadata
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.