Evidence map›Paper›PMID 15735674›Full record

ArticleOncogene2005

ILK mediates actin filament rearrangements and cell migration and invasion through PI3K/Akt/Rac1 signaling.

Yong Qian, Xiaosong Zhong, Daniel C Flynn, Jenny Z Zheng, Meng Qiao, Chuanyue Wu, Shoukat Dedhar, Xianglin Shi, Bing-Hua Jiang

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

68 citing papers in PubMed, 144 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
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  9. Review
  10. Article
  11. UsingFrontiers in cell and developmental biology · 2022
    Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Extracellular Matrix in Regulation of Contractile System in Cardiomyocytes.International journal of molecular sciences · 2019
    Review
  20. Review

8 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

9 authors at 4 institutions in 2 countries.

Yong QianPathology and Physiology Research Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26506, USA. yaq2@cdc.gov
Xiaosong Zhong
Daniel C Flynn
Jenny Z Zheng
Meng Qiao
Chuanyue Wu
Shoukat Dedhar
Xianglin Shi
Bing-Hua Jiang
West Virginia University · USNational Institute for Occupational Safety and Health · USUniversity of British Columbia · CAUniversity of Pittsburgh · US

Funding

THE ROLE OF HEF1 PROTEIN IN INVASION OF METASTATIC BREAST CANCERP20RR016440 · NCRR · WEST VIRGINIA UNIVERSITY · PI CUFF, CHRISTOPHER F · 2001 to 2010
$22.8M
PINCH-1 Interactions and FunctionsR01GM065188 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI WU, CHUANYUE · 2002 to 2014
$3.3M
AFAP-110 regulates signals that affect F-actinR01CA060731 · NCI · WEST VIRGINIA UNIVERSITY · PI HOLT, JEFFREY T · 1999 to 2012
$3.3M
The PINCH-ILK-parvin complexes in glomerular cellsR01DK054639 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI WU, CHUANYUE · 1998 to 2010
$3.2M
PP60SRC BINDING PROTEIN AFAP-110R29CA060731 · NCI · WEST VIRGINIA UNIVERSITY · PI FLYNN, DANIEL · 1994 to 1998
–
NCI NIH HHS CA60731NCRR NIH HHS RR16440NIDDK NIH HHS DK54639NIGMS NIH HHS GM65188
6 · The paper itself

Abstract

One of the hallmarks of integrin signaling is an increase in cell migration and invasion, both of which are associated with actin filament rearrangements. Integrin-linked kinase (ILK) is a cytoplasmic effector of integrin receptors. ILK is known to be involved in multiple cellular functions. However, the signaling pathways involved in ILK-mediated cellular structure and motility remain to be elucidated. Here, we have demonstrated that overexpression of ILK was sufficient to induce actin filament rearrangements, to form cell motility structures, and to increase cell migration and invasion in a phosphatidylinositol 3-kinase (PI3K)-dependent manner. This corresponds with the activation of both Akt and p70 ribosomal protein S6 kinase (p70S6K1). Overexpression of dominant-negative mutants of Akt inhibited ILK-dependent activation of p70S6K1, indicating that Akt is upstream of p70S6K1 in response to ILK signaling. Overexpression of ILK was sufficient to induce Rac1 activation, which was abolish by a PI3K inhibitor, indicating that Rac1 activity is involved in ILK signaling in a PI3K dependent manner. Inhibition of Akt, Rac1, or p70S6K1 inhibited the effects of ILK on actin filaments and cell migration, suggesting a regulatory role of the PI3K/Akt/p70S6K1/Rac1 signaling pathway in response to ILK signaling. We have shown that overexpression of a dominant-negative ILK was sufficient to abolish fibronectin peptide (PHSRN)-induced rearrangements of actin filaments and cell migration and invasion. Taken together, our results identify a mechanism through which ILK can regulate both integrin-associated rearrangements of actin filaments and cell migration and invasion at the integrin receptor-proximal region.

Indexed as

AnimalsBlotting, Westerncdc42 GTP-Binding ProteinCell MovementChickensCytoplasmEnzyme ActivationFibroblastsFibronectinsGenes, DominantHumansIntegrinsMicroscopy, FluorescenceMutationPhosphatidylinositol 3-KinasesPhosphorylationAKT1 protein, humancdc42 GTP-Binding ProteinFibronectinsIntegrinsPhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktrac1 GTP-Binding ProteinRibosomal Protein S6 Kinases, 70-kDaScaffold Protein ILK

Identifiers

PMID15735674
OpenAlexW2087856422

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.