Competition amongst Eph receptors regulates contact inhibition of locomotion and invasiveness in prostate cancer cells

Normal migrating cells exhibit contact inhibition of locomotion (CIL) when meeting a neighbouring cell, but metastatic cancer cells lose this inhibition. Interactions btween ephrin and ephrin receptors are now shown to underlie CIL in migrating cells. Metastatic cancer cells typically fail to halt m...

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Published inNature cell biology Vol. 12; no. 12; pp. 1194 - 1204
Main Authors Astin, Jonathan W., Batson, Jennifer, Kadir, Shereen, Charlet, Jessica, Persad, Raj A., Gillatt, David, Oxley, Jon D., Nobes, Catherine D.
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.12.2010
Nature Publishing Group
Subjects
631/80/84
631/80/86
692/699/67/589/466
Biomedical and Life Sciences
Cancer cells
Cancer Research
Care and treatment
cdc42 GTP-Binding Protein - metabolism
Cell Adhesion
Cell adhesion & migration
Cell Biology
Cell Line, Tumor
Cell Movement
Contact Inhibition
Control
Developmental Biology
Endothelial Cells - metabolism
Ephrin-B2 - metabolism
Fibroblasts
Fibroblasts - metabolism
Gene Knockdown Techniques
Genetic aspects
Health aspects
Humans
Inhibition
Invasiveness
Kinases
Life Sciences
Ligands
Male
Metastasis
Microscopy
Prostate cancer
Prostatic Neoplasms - pathology
Receptors, Eph Family - metabolism
Rocks
Signal Transduction
Stem Cells
United Kingdom
United Kingdom > UK
Online AccessGet full text
ISSN1465-7392
1476-4679
1476-4679
DOI10.1038/ncb2122

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Abstract Normal migrating cells exhibit contact inhibition of locomotion (CIL) when meeting a neighbouring cell, but metastatic cancer cells lose this inhibition. Interactions btween ephrin and ephrin receptors are now shown to underlie CIL in migrating cells. Metastatic cancer cells typically fail to halt migration on contact with non-cancer cells. This invasiveness is in contrast to normal mesenchymal cells that retract on contact with another cell. Why cancer cells are defective in contact inhibition of locomotion is not understood. Here, we analyse the dynamics of prostate cancer cell lines co-cultured with fibroblasts, and demonstrate that a combinatorial code of Eph receptor activation dictates whether cell migration will be contact inhibited. The unimpeded migration of metastatic PC-3 cells towards fibroblasts is dependent on activation of EphB3 and EphB4 by ephrin-B2, which we show activates Cdc42 and cell migration. Knockdown of EphB3 and EphB4 restores contact inhibition of locomotion to PC-3 cells. Conversely, homotypic collisions between two cancer cells results in contact inhibition of locomotion, mediated by EphA–Rho–Rho kinase (ROCK) signalling. Thus, the migration of cancer cells can switch from restrained to invasive, depending on the Eph-receptor profile of the cancer cell and the reciprocal ephrin ligands expressed by neighbouring cells.
AbstractList Normal migrating cells exhibit contact inhibition of locomotion (CIL) when meeting a neighbouring cell, but metastatic cancer cells lose this inhibition. Interactions btween ephrin and ephrin receptors are now shown to underlie CIL in migrating cells. Metastatic cancer cells typically fail to halt migration on contact with non-cancer cells. This invasiveness is in contrast to normal mesenchymal cells that retract on contact with another cell. Why cancer cells are defective in contact inhibition of locomotion is not understood. Here, we analyse the dynamics of prostate cancer cell lines co-cultured with fibroblasts, and demonstrate that a combinatorial code of Eph receptor activation dictates whether cell migration will be contact inhibited. The unimpeded migration of metastatic PC-3 cells towards fibroblasts is dependent on activation of EphB3 and EphB4 by ephrin-B2, which we show activates Cdc42 and cell migration. Knockdown of EphB3 and EphB4 restores contact inhibition of locomotion to PC-3 cells. Conversely, homotypic collisions between two cancer cells results in contact inhibition of locomotion, mediated by EphA–Rho–Rho kinase (ROCK) signalling. Thus, the migration of cancer cells can switch from restrained to invasive, depending on the Eph-receptor profile of the cancer cell and the reciprocal ephrin ligands expressed by neighbouring cells.
Metastatic cancer cells typically fail to halt migration on contact with non-cancer cells. This invasiveness is in contrast to normal mesenchymal cells that retract on contact with another cell. Why cancer cells are defective in contact inhibition of locomotion is not understood. Here, we analyse the dynamics of prostate cancer cell lines co-cultured with fibroblasts, and demonstrate that a combinatorial code of Eph receptor activation dictates whether cell migration will be contact inhibited. The unimpeded migration of metastatic PC-3 cells towards fibroblasts is dependent on activation of EphB3 and EphB4 by ephrin-B2, which we show activates Cdc42 and cell migration. Knockdown of EphB3 and EphB4 restores contact inhibition of locomotion to PC-3 cells. Conversely, homotypic collisions between two cancer cells results in contact inhibition of locomotion, mediated by EphARho-Rho kinase (ROCK) signalling. Thus, the migration of cancer cells can switch from restrained to invasive, depending on the Eph-receptor profile of the cancer cell and the reciprocal ephrin ligands expressed by neighbouring cells.
Metastatic cancer cells typically fail to halt migration on contact with non-cancer cells. This invasiveness is in contrast to normal mesenchymal cells that retract on contact with another cell. Why cancer cells are defective in contact inhibition of locomotion is not understood. Here, we analyse the dynamics of prostate cancer cell lines co-cultured with fibroblasts, and demonstrate that a combinatorial code of Eph receptor activation dictates whether cell migration will be contact inhibited. The unimpeded migration of metastatic PC-3 cells towards fibroblasts is dependent on activation of EphB3 and EphB4 by ephrin-B2, which we show activates Cdc42 and cell migration. Knockdown of EphB3 and EphB4 restores contact inhibition of locomotion to PC-3 cells. Conversely, homotypic collisions between two cancer cells results in contact inhibition of locomotion, mediated by EphA-Rho-Rho kinase (ROCK) signalling. Thus, the migration of cancer cells can switch from restrained to invasive, depending on the Eph-receptor profile of the cancer cell and the reciprocal ephrin ligands expressed by neighbouring cells.
Metastatic cancer cells typically fail to halt migration on contact with non-cancer cells. This invasiveness is in contrast to normal mesenchymal cells that retract on contact with another cell. Why cancer cells are defective in contact inhibition of locomotion is not understood. Here, we analyse the dynamics of prostate cancer cell lines co-cultured with fibroblasts, and demonstrate that a combinatorial code of Eph receptor activation dictates whether cell migration will be contact inhibited. The unimpeded migration of metastatic PC-3 cells towards fibroblasts is dependent on activation of EphB3 and EphB4 by ephrin-B2, which we show activates Cdc42 and cell migration. Knockdown of EphB3 and EphB4 restores contact inhibition of locomotion to PC-3 cells. Conversely, homotypic collisions between two cancer cells results in contact inhibition of locomotion, mediated by EphA-Rho-Rho kinase (ROCK) signalling. Thus, the migration of cancer cells can switch from restrained to invasive, depending on the Eph-receptor profile of the cancer cell and the reciprocal ephrin ligands expressed by neighbouring cells.Metastatic cancer cells typically fail to halt migration on contact with non-cancer cells. This invasiveness is in contrast to normal mesenchymal cells that retract on contact with another cell. Why cancer cells are defective in contact inhibition of locomotion is not understood. Here, we analyse the dynamics of prostate cancer cell lines co-cultured with fibroblasts, and demonstrate that a combinatorial code of Eph receptor activation dictates whether cell migration will be contact inhibited. The unimpeded migration of metastatic PC-3 cells towards fibroblasts is dependent on activation of EphB3 and EphB4 by ephrin-B2, which we show activates Cdc42 and cell migration. Knockdown of EphB3 and EphB4 restores contact inhibition of locomotion to PC-3 cells. Conversely, homotypic collisions between two cancer cells results in contact inhibition of locomotion, mediated by EphA-Rho-Rho kinase (ROCK) signalling. Thus, the migration of cancer cells can switch from restrained to invasive, depending on the Eph-receptor profile of the cancer cell and the reciprocal ephrin ligands expressed by neighbouring cells.
Audience Academic
Author Kadir, Shereen
Nobes, Catherine D.
Gillatt, David
Batson, Jennifer
Persad, Raj A.
Astin, Jonathan W.
Charlet, Jessica
Oxley, Jon D.
Author_xml – sequence: 1
  givenname: Jonathan W.
  surname: Astin
  fullname: Astin, Jonathan W.
  organization: School of Biochemistry, University of Bristol
– sequence: 2
  givenname: Jennifer
  surname: Batson
  fullname: Batson, Jennifer
  organization: School of Biochemistry, University of Bristol
– sequence: 3
  givenname: Shereen
  surname: Kadir
  fullname: Kadir, Shereen
  organization: School of Biochemistry, University of Bristol
– sequence: 4
  givenname: Jessica
  surname: Charlet
  fullname: Charlet, Jessica
  organization: School of Biochemistry, University of Bristol
– sequence: 5
  givenname: Raj A.
  surname: Persad
  fullname: Persad, Raj A.
  organization: Bristol Urological Institute, Southmead Hospital
– sequence: 6
  givenname: David
  surname: Gillatt
  fullname: Gillatt, David
  organization: Bristol Urological Institute, Southmead Hospital
– sequence: 7
  givenname: Jon D.
  surname: Oxley
  fullname: Oxley, Jon D.
  organization: Department of Cellular Pathology, Southmead Hospital
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  givenname: Catherine D.
  surname: Nobes
  fullname: Nobes, Catherine D.
  email: Catherine.Nobes@bristol.ac.uk
  organization: School of Biochemistry, University of Bristol, School of Physiology and Pharmacology, University of Bristol
BackLink https://www.ncbi.nlm.nih.gov/pubmed/21076414$$D View this record in MEDLINE/PubMed
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Snippet Normal migrating cells exhibit contact inhibition of locomotion (CIL) when meeting a neighbouring cell, but metastatic cancer cells lose this inhibition....
Metastatic cancer cells typically fail to halt migration on contact with non-cancer cells. This invasiveness is in contrast to normal mesenchymal cells that...
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StartPage 1194
SubjectTerms 631/80/84
631/80/86
692/699/67/589/466
Biomedical and Life Sciences
Cancer cells
Cancer Research
Care and treatment
cdc42 GTP-Binding Protein - metabolism
Cell Adhesion
Cell adhesion & migration
Cell Biology
Cell Line, Tumor
Cell Movement
Contact Inhibition
Control
Developmental Biology
Endothelial Cells - metabolism
Ephrin-B2 - metabolism
Fibroblasts
Fibroblasts - metabolism
Gene Knockdown Techniques
Genetic aspects
Health aspects
Humans
Inhibition
Invasiveness
Kinases
Life Sciences
Ligands
Male
Metastasis
Microscopy
Prostate cancer
Prostatic Neoplasms - pathology
Receptors, Eph Family - metabolism
Rocks
Signal Transduction
Stem Cells
Title Competition amongst Eph receptors regulates contact inhibition of locomotion and invasiveness in prostate cancer cells
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https://www.ncbi.nlm.nih.gov/pubmed/21076414
https://www.proquest.com/docview/816191267
https://www.proquest.com/docview/815960558
Volume 12
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