Evidence map›Paper›PMID 27009236›Full record

ArticleScientific reports2016

Receptor activator of NF-κB ligand induces cell adhesion and integrin α2 expression via NF-κB in head and neck cancers.

Tamaki Yamada, Masumi Tsuda, Takanori Wagatsuma, Yoichiro Fujioka, Mari Fujioka, Aya O Satoh, Kosui Horiuchi, Shinya Nishide, Asuka Nanbo, Yasunori Totsuka and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. A link betweenOncotarget · 2017
    Article
  8. BRCA1 and MDM2 as independent blood-based biomarkers of head and neck cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    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

14 authors at 1 institution in 1 country.

Tamaki YamadaDepartment of Cell Physiology, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan.
Masumi TsudaDepartment of Cancer Pathology, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan.
Takanori WagatsumaDepartment of Cell Physiology, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan.
Yoichiro FujiokaDepartment of Cell Physiology, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan.
Mari FujiokaDepartment of Cell Physiology, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan.
Aya O SatohDepartment of Cell Physiology, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan.
Kosui HoriuchiDepartment of Cell Physiology, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan.
Shinya NishideDepartment of Cell Physiology, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan.
Asuka NanboDepartment of Cell Physiology, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan.
Yasunori TotsukaLaboratory of Oral and Maxillofacial Surgery, Hokkaido University Graduate School of Dental Medicine, Sapporo 060-8586, Japan.
Hisashi HagaTransdisciplinary Life Science Course, Faculty of Advanced Life Science, Hokkaido University, Sapporo 060-0810, Japan.
Shinya TanakaDepartment of Cancer Pathology, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan.
Masanobu ShindohDivision of Oral Pathobiological Science, Hokkaido University Graduate School of Dental Medicine, Sapporo 060-8586, Japan.
Yusuke OhbaDepartment of Cell Physiology, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan.
Hokkaido University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular interactions with the extracellular matrix play critical roles in tumor progression. We previously reported that receptor activator of NF-κB ligand (RANKL) specifically facilitates head and neck squamous cell carcinoma (HNSCC) progression in vivo. Here, we report a novel role for RANKL in the regulation of cell adhesion. Among the major type I collagen receptors, integrin α2 was significantly upregulated in RANKL-expressing cells, and its knockdown suppressed cell adhesion. The mRNA abundance of integrin α2 positively correlated with that of RANKL in human HNSCC tissues. We also revealed that RANK-NF-κB signaling mediated integrin α2 expression in an autocrine/paracrine manner. Interestingly, the amount of active integrin β1 on the cell surface was increased in RANKL-expressing cells through the upregulation of integrin α2 and endocytosis. Moreover, the RANK-integrin α2 pathway contributed to RANKL-dependent enhanced survival in a collagen gel and inhibited apoptosis in a xenograft model, demonstrating an important role for RANKL-mediated cell adhesion in three-dimensional environments.

Indexed as

AnimalsCarcinoma, Squamous CellCell AdhesionCell Line, TumorCell SurvivalGene Expression Regulation, NeoplasticHead and Neck NeoplasmsHumansIntegrin alpha2MiceNeoplasm TransplantationNF-kappa BRANK LigandSignal TransductionIntegrin alpha2NF-kappa BRANK LigandTNFSF11 protein, human

Identifiers

PMID27009236
PMCPMC4806381
OpenAlexW2324717041

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Registered trials

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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.