Evidence map›Paper›PMID 21478912›Full record

ArticleOncogene2011

Loss of AF6/afadin, a marker of poor outcome in breast cancer, induces cell migration, invasiveness and tumor growth.

G Fournier, O Cabaud, E Josselin, A Chaix, J Adélaïde, D Isnardon, A Restouin, R Castellano, P Dubreuil, M Chaffanet and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.6field-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

30 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Afadin Downregulation byFrontiers in microbiology · 2018
    Article
  14. Article
  15. Genome-Wide miRNA Analysis Identifies miR-188-3p as a Novel Prognostic Marker and Molecular Factor Involved in Colorectal Carcinogenesis.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017
    Article
  16. Article
  17. Article
  18. Article
  19. Afadin is localized at cell-cell contact sites in mesangial cells and regulates migratory polarity.Laboratory investigation; a journal of technical methods and pathology · 2016
    Article
  20. 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

12 authors at 3 institutions in 1 country.

G FournierInserm, UMR 891, Laboratoire d'oncologie moléculaire, CRCM, Marseille, France.
O Cabaud
E Josselin
A Chaix
J Adélaïde
D Isnardon
A Restouin
R Castellano
P Dubreuil
M Chaffanet
D Birnbaum
M Lopez
Inserm · FRInstitut Paoli-Calmettes · FRInstitut de Neurobiologie de la Méditerranée · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Afadin/AF6, an F-actin-binding protein, is ubiquitously expressed in epithelia and has a key role during development, through its regulatory role in cell-cell junction organization. Afadin loss of expression in 15% of breast carcinoma is associated with adverse prognosis and increased risk of metastatic relapse. To determine the role of afadin in breast cancer, we studied the functional consequences of afadin protein extinction using in vitro and in vivo models. Three different breast cancer cell lines representative of the major molecular subtypes were stably repressed for afadin expression (knockdown of afadin (afadin KD)) using RNA interference. Collective and individual migrations as well as Matrigel invasion were markedly increased in afadin KD cells. Heregulin-β1 (HRG-β1)-induced migration and invasion were increased by twofold in afadin KD cells. Conversely, ectopic expression of afadin in the afadin-negative T47D cell line inhibited spontaneous and HRG-β1-induced migrations. RAS/MAPK and SRC kinase pathways were activated in afadin KD cells. Activation levels positively correlated with migration and invasion strength. Use of MEK1/2 (U0126) and SRC kinases (SU6656) inhibitors reduced afadin-dependent migration and invasion. Afadin extinction in the SK-BR-3 cell line markedly accelerated tumor growth development in mouse mammary gland and lung metastasis formation. These results may explain why the loss of afadin expression in tumors correlates with high tumor size and poor metastasis-free survival in patients.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsBreast NeoplasmsCell Line, TumorCell MovementCell ProliferationFemaleHumansKinesinsMAP Kinase Signaling SystemMiceMice, Inbred NODMice, SCIDMicrofilament ProteinsMyosinsNeoplasm InvasivenessafadinAFDN protein, humanAfdn protein, mouseKinesinsMicrofilament ProteinsMyosins

Identifiers

PMID21478912
OpenAlexW1969076427

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.