Evidence map›Paper›PMID 23139833›Full record

ArticlePloS one2012

L-carnitine is an endogenous HDAC inhibitor selectively inhibiting cancer cell growth in vivo and in vitro.

Hongbiao Huang, Ningning Liu, Haiping Guo, Siyan Liao, Xiaofen Li, Changshan Yang, Shouting Liu, Wenbin Song, Chunjiao Liu, Lixia Guan and 6 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 5% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
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  5. Article
  6. Review
  7. Histone acylation at a glance.Journal of cell science · 2024
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
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  14. Radiation-induced Adaptive Response: New Potential for Cancer Treatment.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020
    Review
  15. Review
  16. Review
  17. Review
  18. Article
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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

16 authors at 2 institutions in 2 countries.

Hongbiao HuangProtein Modification and Degradation Lab, Department of Pathophysiology, Guangzhou Medical College, Guangdong, People's Republic of China.
Ningning Liu
Haiping Guo
Siyan Liao
Xiaofen Li
Changshan Yang
Shouting Liu
Wenbin Song
Chunjiao Liu
Lixia Guan
Bing Li
Li Xu
Change Zhang
Xuejun Wang
Q Ping Dou
Jinbao Liu
Guangzhou Medical University · CNUniversity of South Dakota · US

Funding

Ubiquitin receptors and cardiac proteotoxicityR01HL072166 · NHLBI · UNIVERSITY OF SOUTH DAKOTA · PI WANG, XUEJUN · 2003 to 2023
$6.9M
The COP9 SIgnalosome in the HeartR01HL085629 · NHLBI · UNIVERSITY OF SOUTH DAKOTA · PI WANG, XUEJUN · 2006 to 2019
$4.7M
NHLBI NIH HHS R01 HL072166NHLBI NIH HHS R01HL072166NHLBI NIH HHS R01 HL085629NHLBI NIH HHS R01HL085629
6 · The paper itself

Abstract

L-carnitine (LC) is generally believed to transport long-chain acyl groups from fatty acids into the mitochondrial matrix for ATP generation via the citric acid cycle. Based on Warburg's theory that most cancer cells mainly depend on glycolysis for ATP generation, we hypothesize that, LC treatment would lead to disturbance of cellular metabolism and cytotoxicity in cancer cells. In this study, Human hepatoma HepG2, SMMC-7721 cell lines, primary cultured thymocytes and mice bearing HepG2 tumor were used. ATP content was detected by HPLC assay. Cell cycle, cell death and cell viability were assayed by flow cytometry and MTS respectively. Gene, mRNA expression and protein level were detected by gene microarray, Real-time PCR and Western blot respectively. HDAC activities and histone acetylation were detected both in test tube and in cultured cells. A molecular docking study was carried out with CDOCKER protocol of Discovery Studio 2.0 to predict the molecular interaction between L-carnitine and HDAC. Here we found that (1) LC treatment selectively inhibited cancer cell growth in vivo and in vitro; (2) LC treatment selectively induces the expression of p21(cip1) gene, mRNA and protein in cancer cells but not p27(kip1); (4) LC increases histone acetylation and induces accumulation of acetylated histones both in normal thymocytes and cancer cells; (5) LC directly inhibits HDAC I/II activities via binding to the active sites of HDAC and induces histone acetylation and lysine-acetylation accumulation in vitro; (6) LC treatment induces accumulation of acetylated histones in chromatin associated with the p21(cip1) gene but not p27(kip1) detected by ChIP assay. These data support that LC, besides transporting acyl group, works as an endogenous HDAC inhibitor in the cell, which would be of physiological and pathological importance.

Indexed as

AcetylationAdenosine TriphosphateAnimalsCarnitineCell Line, TumorCell ProliferationChromatinCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Gene Expression Regulation, NeoplasticHistone Deacetylase InhibitorsHistone DeacetylasesHistonesHumansMaleMiceAdenosine TriphosphateCarnitineChromatinCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Histone Deacetylase InhibitorsHistone DeacetylasesHistonesRNA, Messenger

Identifiers

PMID23139833
PMCPMC3489732
OpenAlexW1976053959

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.