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

(2013) FASEB JOURNAL. 27(1). p.123-134
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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.
Keywords
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

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MLA
Rochelle, Tristan, et al. “P210bcr-Abl Induces Amoeboid Motility by Recruiting ADF/Destrin through RhoA/ROCK1.” FASEB JOURNAL, vol. 27, no. 1, 2013, pp. 123–34, doi:10.1096/fj.12-205112.
APA
Rochelle, T., Daubon, T., Van Troys, M., Harnois, T., WATERSCHOOT, D., Ampe, C., … Constantin, B. (2013). p210bcr-abl induces amoeboid motility by recruiting ADF/destrin through RhoA/ROCK1. FASEB JOURNAL, 27(1), 123–134. https://doi.org/10.1096/fj.12-205112
Chicago author-date
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): 123–34. https://doi.org/10.1096/fj.12-205112.
Chicago author-date (all authors)
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. doi:10.1096/fj.12-205112.
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.
IEEE
[1]
T. Rochelle et al., “p210bcr-abl induces amoeboid motility by recruiting ADF/destrin through RhoA/ROCK1,” FASEB JOURNAL, vol. 27, no. 1, pp. 123–134, 2013.
@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}},
  keywords     = {{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://doi.org/10.1096/fj.12-205112}},
  volume       = {{27}},
  year         = {{2013}},
}

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