Evidence map›Paper›PMID 15048094›Full record

ArticleOncogene2004

Mutant alpha-actinin-4 promotes tumorigenicity and regulates cell motility of a human lung carcinoma.

Jeanne Menez, Béatrice Le Maux Chansac, Guillaume Dorothée, Isabelle Vergnon, Abdelali Jalil, Marie-France Carlier, Salem Chouaib, Fathia Mami-Chouaib

Abstract read
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In one paragraph

Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Differential expressions of BMPR1α, ACTN4α and FABP7 in Hirschsprung disease.International journal of clinical and experimental pathology · 2014
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Motility-related actinin alpha-4 is associated with advanced and metastatic ovarian carcinoma.Laboratory investigation; a journal of technical methods and pathology · 2008
    Article
  17. Article
  18. A retrovirus-based protein complementation assay screen reveals functional AKT1-binding partners.Proceedings of the National Academy of Sciences of the United States of America · 2006
    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

8 authors at 3 institutions in 1 country.

Jeanne MenezLaboratoire Cytokines et Immunologie des tumeurs Humaines, U487 INSERM, Institut Fédératif de Recherche 54, Institut Gustave Roussy, F-94805 Villejuif Cedex, France.
Béatrice Le Maux Chansac
Guillaume Dorothée
Isabelle Vergnon
Abdelali Jalil
Marie-France Carlier
Salem Chouaib
Fathia Mami-Chouaib
Inserm · FRInstitut Gustave Roussy · FRCentre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The precise role of alpha-actinin-4 encoding gene (ACTN4) is not very well understood. It has been reported to elicit tumor suppressor activity and to regulate cellular motility. To further assess the function of human ACTN4, we studied a lung carcinoma cell line expressing a mutated alpha-actinin-4, which is recognized as a tumor antigen by autologous CD8(+) cytotoxic T lymphocytes (CTL). Confocal immunofluorescence microscopy indicated that, while wild-type (WT) alpha-actinin-4 stains into actin cytoskeleton and cell surface ruffles, the mutated protein is only dispersed in the cytoplasm of the lung carcinoma cells. This loss of association with the cell surface did not appear to correlate with a decrease in in vitro alpha-actinin-4 crosslinking to filamentous (F)-actin. Interestingly, experiments using cell lines stably expressing ACTN4 demonstrated that as opposed to WT gene, mutant ACTN4 was unable to inhibit tumor cell growth in vitro and in vivo. Moreover, the expression of mutant alpha-actinin-4 resulted in the loss of tumor cell capacity to migrate. The identification of an inactivating mutation in ACTN4 emphasizes its role as a tumor suppressor gene and underlines the involvement of cytoskeleton alteration in tumor development and metastasis.

Indexed as

Microfilament ProteinsMutationActininActinsAmino Acid SequenceAnimalsCell DivisionCell Line, TumorCell MembraneCell MovementCloning, MolecularCytoplasmCytoskeletonDNA, ComplementaryDose-Response Relationship, DrugHumansActininActinsACTN4 protein, humanActn4 protein, mouseDNA, ComplementaryMicrofilament Proteins

Identifiers

PMID15048094
OpenAlexW1983250148

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.