Evidence map›Paper›PMID 27015362›Full record

ArticleOncotarget2016

Cellular apoptosis susceptibility (CAS) is linked to integrin β1 and required for tumor cell migration and invasion in hepatocellular carcinoma (HCC).

Juliane Winkler, Stephanie Roessler, Carsten Sticht, Amanda L DiGuilio, Elisabeth Drucker, Kerstin Holzer, Eva Eiteneuer, Esther Herpel, Kai Breuhahn, Norbert Gretz and 3 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Friend or foe? The elusive role of hepatic stellate cells in liver cancer.Nature reviews. Gastroenterology & hepatology · 2023
    Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. C1GALT1 in health and disease.Oncology letters · 2021
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Roles of the CSE1L-mediated nuclear import pathway in epigenetic silencing.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  14. 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

13 authors at 4 institutions in 2 countries.

Juliane WinklerInstitute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
Stephanie RoesslerInstitute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
Carsten StichtMedical Research Centre, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany.
Amanda L DiGuilioDepartment of Chemistry, Chemical Biology and Biomedical Engineering, Stevens Institute of Technology, Hoboken, NJ, USA.
Elisabeth DruckerInstitute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
Kerstin HolzerInstitute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
Eva EiteneuerInstitute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
Esther HerpelInstitute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
Kai BreuhahnInstitute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
Norbert GretzMedical Research Centre, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany.
Peter SchirmacherInstitute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
Alessandro OriEuropean Molecular Biology Laboratory (EMBL), Structural and Computational Biology Unit, Heidelberg, Germany.
Stephan SingerInstitute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
Heidelberg University · DELeibniz Institute on Aging - Fritz Lipmann Institute (FLI) · DEStevens Institute of Technology · USUniversity Hospital Heidelberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Importins and exportins represent an integral part of the nucleocytoplasmic transport machinery with fundamental importance for eukaryotic cell function. A variety of malignancies including hepatocellular carcinoma (HCC) show de-regulation of nuclear transport factors such as overexpression of the exportin Cellular Apoptosis Susceptibility (CAS). The functional implications of CAS in hepatocarcinogenesis remain, however, poorly understood. Here we integrated proteomics, transcriptomics and functional assays with patient data to further characterize the role of CAS in HCC. By analyzing ~ 1700 proteins using quantitative mass spectrometry in HCC cells we found that CAS depletion by RNAi leads to de-regulation of integrins, particularly down-regulation of integrin β1. Consistent with this finding, CAS knockdown resulted in substantially reduced migration and invasion of HCC cell lines as analyzed by 2D 'scratch' and invasion chamber assays, respectively. Supporting the potential in vivo relevance, high expression levels of CAS in HCC tissue samples were associated with macroangioinvasion and poorer patient outcome. Our data suggest a previously unanticipated link between CAS and integrin signaling which correlates with an aggressive HCC phenotype.

Indexed as

Carcinoma, HepatocellularCell MovementCellular Apoptosis Susceptibility ProteinGene Expression Regulation, NeoplasticHumansIntegrin beta1Liver NeoplasmsNeoplasm InvasivenessCellular Apoptosis Susceptibility ProteinIntegrin beta1CASHCCintegrin β1migrationnuclear transport

Identifiers

PMID27015362
PMCPMC5008409
OpenAlexW2344702307

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.