Evidence map›Paper›PMID 11244511›Full record

ArticleOncogene2001

Inhibition of integrin linked kinase (ILK) suppresses beta-catenin-Lef/Tcf-dependent transcription and expression of the E-cadherin repressor, snail, in APC-/- human colon carcinoma cells.

C Tan, P Costello, J Sanghera, D Dominguez, J Baulida, A G de Herreros, S Dedhar

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In one paragraph

Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
7.3field-weighted citation impact, top 2% 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

92 citing papers in PubMed, 248 citations in OpenAlex.

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  20. Integrin-linked kinase regulates cadherin switch in bladder cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article

32 more citing papers are in PubMed but not listed here.

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 3 institutions in 2 countries.

C TanBC Cancer Agency and Jack Bell Research Centre, 2660 Oak Street, Vancouver, BC V6H 3Z6, Canada.
P Costello
J Sanghera
D Dominguez
J Baulida
A G de Herreros
S Dedhar
Universitat Pompeu Fabra · ESUniversity of British Columbia · CABC Cancer Agency · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Loss of functional adenomatous polyposis coli (APC) protein results in the stabilization of cytosolic beta-catenin and activation of genes that are responsive to Lef/Tcf family transcription factors. We have recently shown that an independent cell adhesion and integrin linked kinase (ILK)-dependent pathway can also activate beta-catenin/LEF mediated gene transcription and downregulate E-cadherin expression. In addition, ILK activity and expression are elevated in adenomatous polyposis and colon carcinomas. To examine the role of this pathway in the background of APC mutations we inhibited ILK activity in APC-/- human colon carcinoma cell lines. In all cases, inhibition of ILK resulted in substantial inhibition of TCF mediated gene transcription and inhibition of transcription and expression of the TCF regulated gene, cyclin D1. Inhibition of ILK resulted in decreased nuclear beta-catenin expression, and in the inhibition of phosphorylation of GSK-3 and stimulation of its activity, leading to accelerated degradation of beta-catenin. In addition, inhibition of ILK suppressed cell growth in culture as well as growth of human colon carcinoma cells in SCID mice. Strikingly, inhibition of ILK also resulted in the transcriptional stimulation of E-cadherin expression and correlated with the inhibition of gene transcription of snail, a repressor of E-cadherin gene expression. Overexpression of ILK caused a stimulation of expression of snail, but snail expression was found not to be regulated by beta-catenin/Tcf. These data demonstrate that ILK can regulate beta-catenin/TCF and snail transcription factors by distinct pathways. We propose that inhibition of ILK may be a useful strategy in the control of progression of colon as well as other carcinomas. Oncogene (2001) 20, 133 - 140.

Indexed as

Trans-ActivatorsTranscription, GeneticAdenomatous Polyposis ColiAdenomatous Polyposis Coli Proteinbeta CateninCadherinsColonic NeoplasmsCytoskeletal ProteinsDNA-Binding ProteinsGenes, APCHumansIntegrinsLymphoid Enhancer-Binding Factor 1Neoplasm ProteinsProtein Serine-Threonine KinasesRepressor ProteinsAdenomatous Polyposis Coli Proteinbeta CateninCadherinsCTNNB1 protein, humanCytoskeletal ProteinsDNA-Binding ProteinsIntegrinsLymphoid Enhancer-Binding Factor 1Neoplasm ProteinsProtein Serine-Threonine KinasesRepressor ProteinsScaffold Protein ILKSnail Family Transcription FactorsTrans-ActivatorsTranscription Factors

Identifiers

PMID11244511
OpenAlexW2325413783

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.