Evidence map›Paper›PMID 19935706›Full record

ArticleOncogene2010

Fhit regulates invasion of lung tumor cells.

A Joannes, A Bonnomet, S Bindels, M Polette, C Gilles, H Burlet, J Cutrona, J-M Zahm, P Birembaut, B Nawrocki-Raby

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
0.4field-weighted citation impact, top 37% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Transcriptomic FHITFrontiers in immunology · 2022
    Article
  4. Article
  5. Article
  6. Article
  7. The hallmarks of severe pulmonary arterial hypertension: the cancer hypothesis-ten years later.American journal of physiology. Lung cellular and molecular physiology · 2020
    Review
  8. Article
  9. FHIT, a Novel Modifier Gene in Pulmonary Arterial Hypertension.American journal of respiratory and critical care medicine · 2019
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. The FHIT gene product: tumor suppressor and genome "caretaker".Cellular and molecular life sciences : CMLS · 2014
    Review
  17. Article
  18. Article
  19. 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

10 authors at 4 institutions in 2 countries.

A JoannesINSERM, U903, Reims, France.
A Bonnomet
S Bindels
M Polette
C Gilles
H Burlet
J Cutrona
J-M Zahm
P Birembaut
B Nawrocki-Raby
Inserm · FRUniversité de Reims Champagne-Ardenne · FRUniversity of Liège · BECentre de Recherche en Économie et Statistique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In many types of cancers, the fragile histidine triad (Fhit) gene is frequently targeted by genomic alterations leading to a decrease or loss of gene and protein expression. Fhit has been described as a tumor suppressor gene because of its ability to induce apoptosis and to inhibit proliferation of tumor cells. Moreover, several studies have shown a correlation between the lack of Fhit expression and tumor aggressiveness, thus suggesting that Fhit could be involved in tumor progression. In this study, we explored the potential role of Fhit during tumor cell invasion. We first showed that a low Fhit expression is associated with in vivo and in vitro invasiveness of tumor cells. Then, we showed that Fhit overexpression in Fhit-negative highly invasive NCI-H1299 cells by transfection of Fhit cDNA and Fhit inhibition in Fhit-positive poorly invasive HBE4-E6/E7 cells by transfection of Fhit small interfering RNA induce, respectively, a decrease and an increase in migratory/invasive capacities. These changes in cell behavior were associated with a reorganization of tight and adherens junction molecules and a regulation of matrix metalloproteinase and vimentin expression. These results show that Fhit controls the invasive phenotype of lung tumor cells by regulating the expression of genes associated with epithelial-mesenchymal transition.

Indexed as

Genetic TherapyAcid Anhydride HydrolasesAnimalsApoptosisBiomarkers, TumorBis(5'-adenosyl)triphosphataseCell Line, TumorCyclin-Dependent Kinase Inhibitor p21Gene Expression Regulation, NeoplasticGenetic VectorsHistidineLoss of HeterozygosityLung NeoplasmsMiceMice, NudeNeoplasm InvasivenessAcid Anhydride HydrolasesBiomarkers, TumorBis(5'-adenosyl)triphosphataseCyclin-Dependent Kinase Inhibitor p21HistidineNeoplasm ProteinsRNA, Small InterferingTNF-Related Apoptosis-Inducing LigandTumor Suppressor Proteins

Identifiers

PMID19935706
OpenAlexW2046207355

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.