Evidence map›Paper›PMID 24163426›Full record

ArticleJournal of molecular cell biology2013

A specific cholesterol metabolic pathway is established in a subset of HCCs for tumor growth.

Ming Lu, Xi-Han Hu, Qin Li, Ying Xiong, Guang-Jing Hu, Jia-Jia Xu, Xiao-Nan Zhao, Xi-Xiao Wei, Catherine C Y Chang, Yin-Kun Liu and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of molecular cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 8% 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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

  1. Pooled it
  2. Article
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  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Lipid Metabolism as a Potential Target of Liver Cancer.Journal of hepatocellular carcinoma · 2024
    Review
  12. Review
  13. Article
  14. Comparative Transcriptomic Analysis of Three Common Liver Cell Lines.International journal of molecular sciences · 2023
    Article
  15. Review
  16. Review
  17. Article
  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

15 authors at 4 institutions in 3 countries.

Ming LuState Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
Xi-Han Hu
Qin Li
Ying Xiong
Guang-Jing Hu
Jia-Jia Xu
Xiao-Nan Zhao
Xi-Xiao Wei
Catherine C Y Chang
Yin-Kun Liu
Fa-Jun Nan
Jia Li
Ta-Yuan Chang
Bao-Liang Song
Bo-Liang Li
MRC Laboratory of Molecular Biology · GBChinese Academy of Sciences · CNDartmouth College · USFudan University · CN

Funding

STRUCTURE/FUNCTION ANALYSIS OF ACATR01HL060306 · NHLBI · DARTMOUTH COLLEGE · PI CHANG, TA YUAN · 1998 to 2015
$5.5M
CELL MUTANTS DEFECTIVE IN CHOLESTEROL ESTER FORMATIONR01HL036709 · NHLBI · DARTMOUTH COLLEGE · PI CHANG, TA YUAN · 1986 to 2012
$3.9M
CELL MUTANTS DEFECTIVE IN CHOLESTEROL ESTER FORMATIONR37HL036709 · NHLBI · DARTMOUTH COLLEGE · PI CHANG, TA-YUAN · 1994 to 2003
$1.4M
NHLBI NIH HHS HL36709NHLBI NIH HHS R01 HL036709NHLBI NIH HHS R01 HL060306
6 · The paper itself

Abstract

The liver plays a central role in cholesterol homeostasis. It exclusively receives and metabolizes oxysterols, which are important metabolites of cholesterol and are more cytotoxic than free cholesterol, from all extrahepatic tissues. Hepatocellular carcinomas (HCCs) impair certain liver functions and cause pathological alterations in many processes including cholesterol metabolism. However, the link between an altered cholesterol metabolism and HCC development is unclear. Human ACAT2 is abundantly expressed in intestine and fetal liver. Our previous studies have shown that ACAT2 is induced in certain HCC tissues. Here, by investigating tissue samples from HCC patients and HCC cell lines, we report that a specific cholesterol metabolic pathway, involving induction of ACAT2 and esterification of excess oxysterols for secretion to avoid cytotoxicity, is established in a subset of HCCs for tumor growth. Inhibiting ACAT2 leads to the intracellular accumulation of unesterified oxysterols and suppresses the growth of both HCC cell lines and their xenograft tumors. Further mechanistic studies reveal that HCC-linked promoter hypomethylation is essential for the induction of ACAT2 gene expression. We postulate that specifically blocking this HCC-established cholesterol metabolic pathway may have potential therapeutic applications for HCC patients.

Indexed as

AnimalsCarcinoma, HepatocellularCell Line, TumorCholesterolHep G2 CellsHumansIn Vitro TechniquesLiver NeoplasmsMaleMetabolic Networks and PathwaysMice, NudeXenograft Model Antitumor AssaysCholesterolACAT2CpG methylationHCCinhibition of tumor growthoxysterol secretion

Identifiers

PMID24163426
PMCPMC3841111
OpenAlexW2139983518

What OpenQuestion holds

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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.