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BCL2 interaction with actin in vitro may inhibit cell motility by enhancing actin polymerization.

Publication ,  Journal Article
Ke, H; Zhang, JY; Akiyama, SK; French, JE
Published in: Cell Adh Migr
2011

In addition to its well-defined role as an antagonist in apoptosis, we propose that BCL2 may act as an intracellular suppressor of cell motility and adhesion under certain conditions. Our evidence shows that, when over-expressed in both cancer and non-cancer cells, BCL2 can form a complex with actin and gelsolin that functions to decrease gelsolin-severing activity to increase actin polymerization, and, thus, suppress cell adhesive processes. The linkage between increased BCL2 and increased actin polymerization on the one hand, and suppression of cell adhesion, spreading, and motility on the other hand, is a novel observation that may provide a plausible explanation for why BCL2 over-expression in some tumors is correlated with improved patient survival. In addition, we have identified conditions in vitro in which F-actin polymerization can be increased while cell motility is reduced. These findings underscore the possibility that BCL2 may be involved in modulating cytoskeleton reorganization, and may provide an opportunity to explore signal transduction pathways important for cell adhesion and migration and to develop small molecule therapies for suppression of cancer metastasis.

Duke Scholars

Published In

Cell Adh Migr

DOI

EISSN

1933-6926

Publication Date

2011

Volume

5

Issue

1

Start / End Page

6 / 10

Location

United States

Related Subject Headings

  • Proto-Oncogene Proteins c-bcl-2
  • Polymerization
  • Neoplasm Metastasis
  • Mice
  • Humans
  • Gelsolin
  • Developmental Biology
  • Cytoskeleton
  • Cell Movement
  • Cell Line, Tumor
 

Citation

APA
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ICMJE
MLA
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Ke, H., Zhang, J. Y., Akiyama, S. K., & French, J. E. (2011). BCL2 interaction with actin in vitro may inhibit cell motility by enhancing actin polymerization. Cell Adh Migr, 5(1), 6–10. https://doi.org/10.4161/cam.5.1.13175
Ke, Hengning, Jennifer Y. Zhang, Steven K. Akiyama, and John E. French. “BCL2 interaction with actin in vitro may inhibit cell motility by enhancing actin polymerization.Cell Adh Migr 5, no. 1 (2011): 6–10. https://doi.org/10.4161/cam.5.1.13175.
Ke H, Zhang JY, Akiyama SK, French JE. BCL2 interaction with actin in vitro may inhibit cell motility by enhancing actin polymerization. Cell Adh Migr. 2011;5(1):6–10.
Ke, Hengning, et al. “BCL2 interaction with actin in vitro may inhibit cell motility by enhancing actin polymerization.Cell Adh Migr, vol. 5, no. 1, 2011, pp. 6–10. Pubmed, doi:10.4161/cam.5.1.13175.
Ke H, Zhang JY, Akiyama SK, French JE. BCL2 interaction with actin in vitro may inhibit cell motility by enhancing actin polymerization. Cell Adh Migr. 2011;5(1):6–10.

Published In

Cell Adh Migr

DOI

EISSN

1933-6926

Publication Date

2011

Volume

5

Issue

1

Start / End Page

6 / 10

Location

United States

Related Subject Headings

  • Proto-Oncogene Proteins c-bcl-2
  • Polymerization
  • Neoplasm Metastasis
  • Mice
  • Humans
  • Gelsolin
  • Developmental Biology
  • Cytoskeleton
  • Cell Movement
  • Cell Line, Tumor