Evidence map›Paper›PMID 39581761›Full record

ArticleCancer science2025

Integrin-α5 expression and its role in non-small cell lung cancer progression.

Mirei Ka, Yoko Matsumoto, Takahiro Ando, Munetoshi Hinata, Qian Xi, Yuriko Sugiura, Takahiro Iida, Natsuki Nakagawa, Masakatsu Tokunaga, Kousuke Watanabe and 5 more

Abstract read
In one paragraph

Article in Cancer science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
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

10 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. ITGA5 is overexpressed and promotes tumor progression through SNAI2 in OSCC.Frontiers in cell and developmental biology · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. 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

15 authors.

Mirei KaDivision of Integrative Genomics, The University of Tokyo, Tokyo, Japan.ORCID https://orcid.org/0009-0001-8950-8948
Yoko MatsumotoDepartment of Respiratory Medicine, The University of Tokyo, Tokyo, Japan.
Takahiro AndoDepartment of Respiratory Medicine, The University of Tokyo, Tokyo, Japan.ORCID https://orcid.org/0000-0002-4489-5243
Munetoshi HinataDepartment of Pathology, The University of Tokyo, Tokyo, Japan.
Qian XiDivision of Integrative Genomics, The University of Tokyo, Tokyo, Japan.
Yuriko SugiuraDepartment of Respiratory Medicine, The University of Tokyo, Tokyo, Japan.
Takahiro IidaDepartment of Thoracic Surgery, The University of Tokyo, Tokyo, Japan.
Natsuki NakagawaDepartment of Respiratory Medicine, The University of Tokyo, Tokyo, Japan.
Masakatsu TokunagaDepartment of Respiratory Medicine, The University of Tokyo, Tokyo, Japan.
Kousuke WatanabeNext-Generation Precision Medicine Development Laboratory, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Masanori KawakamiDepartment of Respiratory Medicine, The University of Tokyo, Tokyo, Japan.
Tetsuo UshikuDepartment of Pathology, The University of Tokyo, Tokyo, Japan.
Masaaki SatoDepartment of Thoracic Surgery, The University of Tokyo, Tokyo, Japan.
Katsutoshi OdaDivision of Integrative Genomics, The University of Tokyo, Tokyo, Japan.
Hidenori KageDepartment of Respiratory Medicine, The University of Tokyo, Tokyo, Japan.

Funding

Konica Minolta Imaging Science Foundation
6 · The paper itself

Abstract

Integrins are transmembrane receptors that facilitate cell adhesion to the extracellular matrix and neighboring cells. Aberrant expression of integrins has been associated with tumor progression and metastasis in various cancer types. Integrin alpha-5 (ITGA5) is an integrin subtype that serves as a receptor for fibronectin, fibrinogen, and fibrillin-1. The purpose of this study was to elucidate how ITGA5 expression plays a role in human non-small cell lung cancer (NSCLC). Our clinical data, along with data retrieved from The Cancer Genome Database (TCGA), revealed that high ITGA5 expression in NSCLC patients was associated with a lower recurrence-free survival and overall survival. In our in vitro functional assays, ITGA5 overexpression in human NSCLC cell lines resulted in increased cell size, adhesion, and migration properties, while knockdown of ITGA5 restored the phenotypes. Correspondingly, knockdown and inhibition of ITGA5 in endogenously high-expressing NSCLC cell lines resulted in decreased cell size, adhesion, migration, and proliferation. The antiproliferative effect was also confirmed by a reduction in Ki-67 without discernible changes in apoptosis. Collectively, these findings reveal the significant role of ITGA5 in various functional behaviors in NSCLC, providing a potential therapeutic target for NSCLC patients with high ITGA5 expression.

Indexed as

Carcinoma, Non-Small-Cell LungIntegrin alpha5Lung NeoplasmsApoptosisCell AdhesionCell Line, TumorCell MovementCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansIntegrinsMaleMiddle AgedIntegrin alpha5IntegrinsITGA5 protein, humanadhesionintegrin alpha‐5migrationnon‐small cell lung cancerpostoperative recurrence

Identifiers

PMID39581761
PMCPMC11786322

What OpenQuestion holds

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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.