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p210bcr-abl induces amoeboid motility by recruiting ADF/destrin through RhoA/ROCK1

Tristan Rochelle, Thomas Daubon, Marleen Van Troys UGent, Thomas Harnois, Davy Waterschoot UGent, Christophe Ampe UGent, Lydia Roy, Nicolas Bourmeyster and Bruno Constantin (2013) FASEB JOURNAL. 27(1). p.123-134
abstract
We previously demonstrated that the BcrAbl oncogene, p210(bcr-abl), through its unique GEF domain, specifically activates RhoA and induces spontaneous amoeboid motility. We intend to study the pathways downstream RhoA controlling amoeboid motility. Mouse prolymphoblastic cells (Ba/F3 cell line) expressing different forms of Bcr-Abl were embedded in 3-dimensional (3D) Matrigel to study motility and explore the effects of inhibiting Rho pathway (inhibitors and siRNAs). The phosphorylation levels of cofilin-1 and destrin were analyzed by 2-dimensional electrophoresis. Composition of Bcr-Abl signalplex in different conditions was determined by coimmunoprecipitation. Ba/F3p190 and Ba/F3 expressing a mutant form of p210(bcr-abl) (unable to activate RhoA) cells presented a spontaneous motility, but not an amoeboid type. p210(bcr-abl)-induced amoeboid motility in a 3D matrix requires isoform-specific RhoA/ROCK-1/destrin signaling. Next to the conventional Rho/ROCK/MLC/myosin pathway, this pathway is a crucial determinant for amoeboid motility, specific for the destrin isoform (and not its coexpressed homologue cofilin-1). Also, the presence of destrin (and not cofilin-1) in the p210(bcr-abl) complex is dependent on ROCK1, and this signalplex is required for amoeboid motility. This underscores isoform-specific function within the ADF/cofilin family and provides new insight into Bcr-Abl signaling to amoeboid motility and possible impact on understanding chronic myeloid leukemia progression.
Please use this url to cite or link to this publication:
author
organization
alternative title
p210(bcr-abl) induces amoeboid motility by recruiting ADF/destrin through RhoA/ROCK1
year
type
journalArticle (original)
publication status
published
subject
keyword
cell migration, isoform selectivity, GTPases, actin-binding proteins, signalplex, leukemia, CHRONIC MYELOGENOUS LEUKEMIA, TUMOR-CELL INVASION, ACTIN-DEPOLYMERIZING FACTOR, CHRONIC MYELOID-LEUKEMIA, BCR-ABL ONCOGENE, RHO-GTPASES, CHEMOTACTIC RESPONSE, STRESS FIBERS, LIM-KINASE, MIGRATION
journal title
FASEB JOURNAL
Faseb J.
volume
27
issue
1
pages
123 - 134
Web of Science type
Article
Web of Science id
000313103200013
JCR category
BIOLOGY
JCR impact factor
5.48 (2013)
JCR rank
7/85 (2013)
JCR quartile
1 (2013)
ISSN
0892-6638
DOI
10.1096/fj.12-205112
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
3031238
handle
http://hdl.handle.net/1854/LU-3031238
date created
2012-10-18 13:58:11
date last changed
2013-01-31 16:47:21
@article{3031238,
  abstract     = {We previously demonstrated that the BcrAbl oncogene, p210(bcr-abl), through its unique GEF domain, specifically activates RhoA and induces spontaneous amoeboid motility. We intend to study the pathways downstream RhoA controlling amoeboid motility. Mouse prolymphoblastic cells (Ba/F3 cell line) expressing different forms of Bcr-Abl were embedded in 3-dimensional (3D) Matrigel to study motility and explore the effects of inhibiting Rho pathway (inhibitors and siRNAs). The phosphorylation levels of cofilin-1 and destrin were analyzed by 2-dimensional electrophoresis. Composition of Bcr-Abl signalplex in different conditions was determined by coimmunoprecipitation. Ba/F3p190 and Ba/F3 expressing a mutant form of p210(bcr-abl) (unable to activate RhoA) cells presented a spontaneous motility, but not an amoeboid type. p210(bcr-abl)-induced amoeboid motility in a 3D matrix requires isoform-specific RhoA/ROCK-1/destrin signaling. Next to the conventional Rho/ROCK/MLC/myosin pathway, this pathway is a crucial determinant for amoeboid motility, specific for the destrin isoform (and not its coexpressed homologue cofilin-1). Also, the presence of destrin (and not cofilin-1) in the p210(bcr-abl) complex is dependent on ROCK1, and this signalplex is required for amoeboid motility. This underscores isoform-specific function within the ADF/cofilin family and provides new insight into Bcr-Abl signaling to amoeboid motility and possible impact on understanding chronic myeloid leukemia progression.},
  author       = {Rochelle, Tristan and Daubon, Thomas and Van Troys, Marleen and Harnois, Thomas and Waterschoot, Davy and Ampe, Christophe and Roy, Lydia and Bourmeyster, Nicolas and Constantin, Bruno},
  issn         = {0892-6638},
  journal      = {FASEB JOURNAL},
  keyword      = {cell migration,isoform selectivity,GTPases,actin-binding proteins,signalplex,leukemia,CHRONIC MYELOGENOUS LEUKEMIA,TUMOR-CELL INVASION,ACTIN-DEPOLYMERIZING FACTOR,CHRONIC MYELOID-LEUKEMIA,BCR-ABL ONCOGENE,RHO-GTPASES,CHEMOTACTIC RESPONSE,STRESS FIBERS,LIM-KINASE,MIGRATION},
  language     = {eng},
  number       = {1},
  pages        = {123--134},
  title        = {p210bcr-abl induces amoeboid motility by recruiting ADF/destrin through RhoA/ROCK1},
  url          = {http://dx.doi.org/10.1096/fj.12-205112},
  volume       = {27},
  year         = {2013},
}

Chicago
Rochelle, Tristan, Thomas Daubon, Marleen Van Troys, Thomas Harnois, Davy Waterschoot, Christophe Ampe, Lydia Roy, Nicolas Bourmeyster, and Bruno Constantin. 2013. “P210bcr-abl Induces Amoeboid Motility by Recruiting ADF/destrin Through RhoA/ROCK1.” Faseb Journal 27 (1): 123–134.
APA
Rochelle, T., Daubon, T., Van Troys, M., Harnois, T., Waterschoot, D., Ampe, C., Roy, L., et al. (2013). p210bcr-abl induces amoeboid motility by recruiting ADF/destrin through RhoA/ROCK1. FASEB JOURNAL, 27(1), 123–134.
Vancouver
1.
Rochelle T, Daubon T, Van Troys M, Harnois T, Waterschoot D, Ampe C, et al. p210bcr-abl induces amoeboid motility by recruiting ADF/destrin through RhoA/ROCK1. FASEB JOURNAL. 2013;27(1):123–34.
MLA
Rochelle, Tristan, Thomas Daubon, Marleen Van Troys, et al. “P210bcr-abl Induces Amoeboid Motility by Recruiting ADF/destrin Through RhoA/ROCK1.” FASEB JOURNAL 27.1 (2013): 123–134. Print.