Evidence map›Paper›PMID 16407822›Full record

ArticleOncogene2006

Integrin-linked kinase activity is associated with interleukin-1 alpha-induced progressive behavior of pancreatic cancer and poor patient survival.

H Sawai, Y Okada, H Funahashi, Y Matsuo, H Takahashi, H Takeyama, T Manabe

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.1field-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

28 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Integrin-linked kinase (ILK): the known vs. the unknown and perspectives.Cellular and molecular life sciences : CMLS · 2022
    Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. tsRNA signatures in cancer.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  8. Article
  9. Article
  10. Comparison of ILK and ERP29 expressions in benign and malignant pancreatic lesions and their clinicopathological significances in pancreatic ductal adenocarcinomas.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2016
    Article
  11. Article
  12. Article
  13. Overexpression of ILK1 in breast cancer associates with poor prognosis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Article
  14. Article
  15. ILK and PRDX1 are prognostic markers in squamous cell/adenosquamous carcinomas and adenocarcinoma of gallbladder.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Integrin-linked kinase 1: role in hormonal cancer progression.Frontiers in bioscience (Scholar edition) · 2011
    Review
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.

H SawaiDepartment of Gastroenterological Surgery, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan. cb8h-swi@asahi-net.or.jp
Y Okada
H Funahashi
Y Matsuo
H Takahashi
H Takeyama
T Manabe
Nagoya City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cell adhesion and invasion into extracellular matrix are regulated by integrin-linked kinase (ILK) activity in a phosphatidylinositol 3-kinase (PI3-K)-dependent manner. In this study, we demonstrated that ILK and beta(1)-integrin play important roles in interleukin (IL)-1alpha-induced enhancement of adhesion and invasion of pancreatic cancer cells through p38 mitogen-activated protein kinase (MAPK) signaling pathway and activator protein-1 (AP-1) activation. Alteration of ILK kinase activity controlled IL-1alpha-induced p38 MAPK phosphorylation and its downstream AP-1 activation with subsequent regulation of pancreatic cancer cell adhesion and invasion. Overexpressed ILK enhances the IL-1alpha-induced p38 MAPK phosphorylation more strongly through glycogen synthase kinase 3 (GSK-3) activation, and subsequently induces AP-1 activation, which promotes aggressive capabilities of pancreatic cancer cells. In contrast, knockdown of ILK kinase activity inhibits the IL-1alpha-induced activation of MAPK/AP-1 pathway via inhibition of GSK-3 phosphorylation. In immunohistochemical analysis, statistically significant association between strong expression of ILK and poor prognosis of pancreatic cancer patients were observed, and strong expression of ILK in cancerous tissues can be a significant prognostic indicator of pancreatic cancer patients. Our results suggest that ILK is involved with aggressive capability in pancreatic cancer and that these regulations can be helpful to understand biological processes for a better translational treatment for pancreatic cancer patients.

Indexed as

Cell AdhesionCell Line, TumorDisease ProgressionHumansIntegrin beta1Interleukin-1Neoplasm InvasivenessPancreatic NeoplasmsPrognosisProtein Serine-Threonine KinasesScaffold Protein ILKSurvival AnalysisIntegrin beta1Interleukin-1Protein Serine-Threonine KinasesScaffold Protein ILK

Identifiers

PMID16407822
OpenAlexW2084112964

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.