Evidence map›Paper›PMID 16504015›Full record

ArticleBMC cell biology2006

Interleukin-1alpha enhances the aggressive behavior of pancreatic cancer cells by regulating the alpha6beta1-integrin and urokinase plasminogen activator receptor expression.

Hirozumi Sawai, Yuji Okada, Hitoshi Funahashi, Yoichi Matsuo, Hiroki Takahashi, Hiromitsu Takeyama, Tadao Manabe

Open access · goldAbstract read
In one paragraph

Article in BMC cell biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.5field-weighted citation impact, top 12% 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, 48 citations in OpenAlex.

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  18. Gene expression profiles associated with advanced pancreatic cancer.International journal of clinical and experimental pathology · 2008
    Article
  19. Dose-dependent cross-talk between the transforming growth factor-beta and interleukin-1 signaling pathways.Proceedings of the National Academy of Sciences of the United States of America · 2007
    Article
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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

7 authors at 1 institution in 1 country.

Hirozumi SawaiDepartment of Gastroenterological Surgery, Nagoya City University Graduate School of Medical Sciences, Nagoya 4678601, Japan. cb8h-swi@asahi-net.or.jp
Yuji Okada
Hitoshi Funahashi
Yoichi Matsuo
Hiroki Takahashi
Hiromitsu Takeyama
Tadao Manabe
Nagoya City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn human pancreatic cancer progression, the alpha6beta1-integrin is expressed on cancer cell surface during invasion and metastasis formation. In this study, we investigated whether interleukin (IL)-1alpha induces the alterations of integrin subunits and urokinase plasminogen activator/urokinase plasminogen activator receptor (uPA/uPAR) expression in pancreatic cancer cells. We hypothesize that the alterations of integrin subunits and uPA/uPAR expression make an important role in signaling pathways responsible for biological behavior of pancreatic cancer cells.

resultsIL-1alpha upregulated the expression of alpha6 and beta1 integrins without any alterations of alpha5 and alphav integrins expression. IL-1alpha also induced enhancement in the expression of uPA/uPAR in pancreatic cancer cells. IL-1alpha enhanced the proliferation, adhesion, and migration in pancreatic cancer cells, and IL-1alpha-induced alterations of uPA/uPAR expression correlated with the increased the migration of pancreatic cancer cells. Upregulation of alpha6 integrin subunit and uPA/uPAR correlated with the activation of Ras and downstream extracellular signal-regulated kinase (ERK) pathways. IL-1alpha-induced activation of Ras and downstream ERK can be inhibited by using inhibitory antibodies against alpha6 and beta1 integrin and uPAR, consistent with the inhibition of proliferation, adhesion and migration of pancreatic cancer cells. Immunohistochemical analysis demonstrated a significant association between strong expressions of alpha6 integrin with uPAR in pancreatic cancer specimens. Furthermore, the strong expression of alpha6 integrin and uPAR was found to be independent prognosticator in pancreatic cancer patients.

conclusionBased on these findings, we conclude that IL-1alpha can induce selective upregulation of alpha6beta1-integrin and uPA/uPAR in pancreatic cancer cells and these changes may modulate the aggressive functions of pancreatic cancer.

Indexed as

AgedAged, 80 and overCarcinoma, Pancreatic DuctalCell AdhesionCell DivisionCell Line, TumorCell MovementExtracellular Signal-Regulated MAP KinasesFemaleHumansIntegrin alpha5Integrin alpha6beta1Integrin alphaVIntegrin beta4Interleukin-1LamininExtracellular Signal-Regulated MAP KinasesIntegrin alpha5Integrin alpha6beta1Integrin alphaVIntegrin beta4Interleukin-1LamininNeoplasm ProteinsPLAUR protein, humanProto-Oncogene Proteins p21(ras)Receptors, Cell SurfaceReceptors, Urokinase Plasminogen ActivatorRecombinant Fusion ProteinsUrokinase-Type Plasminogen Activator

Identifiers

PMID16504015
PMCPMC1388210
OpenAlexW2120941190

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.