Evidence map›Paper›PMID 29896915›Full record

ArticleCancer science2018

Role of caveolin-1 in hepatocellular carcinoma arising from non-alcoholic fatty liver disease.

Makoto Takeda, Takanori Sakaguchi, Takanori Hiraide, Yasushi Shibasaki, Yoshifumi Morita, Hirotoshi Kikuchi, Koji Ikegami, Mitsutoshi Setou, Hiroyuki Konno, Hiroya Takeuchi

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 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
1.5field-weighted citation impact, top 19% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
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  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Non-Cirrhotic Liver is Associated with Poor Prognosis of Hepatocellular Carcinoma: A Literature Review.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Review
  11. Review
  12. 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

10 authors at 2 institutions in 3 countries.

Makoto TakedaSecond Department of Surgery, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Takanori SakaguchiSecond Department of Surgery, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Takanori HiraideSecond Department of Surgery, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Yasushi ShibasakiSecond Department of Surgery, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Yoshifumi MoritaSecond Department of Surgery, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Hirotoshi KikuchiSecond Department of Surgery, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Koji IkegamiDepartment of Cellular and Molecular Anatomy, International Mass Imaging Center, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Mitsutoshi SetouDepartment of Cellular and Molecular Anatomy, International Mass Imaging Center, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Hiroyuki KonnoSecond Department of Surgery, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Hiroya TakeuchiSecond Department of Surgery, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Hamamatsu University School of Medicine · JPChinese University of Hong Kong · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The molecular features of hepatocellular carcinoma arising from non-alcoholic fatty liver disease (NAFLD-HCC) are not well known. In this study, we investigated the mechanism by which NAFLD-HCC survives in a fat-rich environment. We found that caveolin (CAV)-1 was overexpressed in clinical specimens from NAFLD-HCC patients. HepG2, HLE, and HuH-7 HCC cell lines showed decreased proliferation in the presence of the saturated fatty acids palmitic acid and stearic acid, although only HLE cells expressed high levels of CAV-1. HLE cells treated with oleic acid (OA) showed robust proliferation, whereas CAV-null HepG2 cells showed reduced proliferation and increased apoptosis. CAV-1 knockdown in HLE cells attenuated the OA-induced increase in proliferation and enhanced apoptosis. Liquid chromatography-tandem mass spectrometry analysis revealed that the levels of OA-containing ceramide, a pro-apoptotic factor, were higher in HepG2 and CAV-1-deficient HLE cells than in HLE cells, suggesting that CAV-1 inhibits apoptosis by decreasing the level of OA-containing ceramide. These results indicate that CAV-1 is important for NAFLD-HCC survival in fatty acid-rich environments and is a potential therapeutic target.

Indexed as

AgedAged, 80 and overApoptosisCarcinoma, HepatocellularCaveolin 1Cell Line, TumorCell ProliferationFatty AcidsFemaleHepatocytesHep G2 CellsHumansLiver NeoplasmsMaleMiddle AgedNon-alcoholic Fatty Liver DiseaseCAV1 protein, humanCaveolin 1Fatty Acidsapoptosiscaveolin-1ceramidehepatocellular carcinomanon-alcoholic fatty liver disease

Identifiers

PMID29896915
PMCPMC6113505
OpenAlexW2808435727

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.