Molecular Biology of the Cell

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
QUICK SEARCH:   [advanced]


     

Originally published as MBC in Press, 10.1091/mbc.E08-03-0319 on May 21, 2008

Vol. 19, Issue 8, 3357-3368, August 2008

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplemental Materials
Right arrow All Versions of this Article:
E08-03-0319v1
19/8/3357    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Related articles in Mol. Biol. Cell
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Google Scholar
Right arrow Articles by Beadle, C.
Right arrow Articles by Canoll, P.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Beadle, C.
Right arrow Articles by Canoll, P.

The Role of Myosin II in Glioma Invasion of the Brain

Christopher Beadle*,{dagger}, Marcela C. Assanah*,{ddagger}, Pascale Monzo§, Richard Vallee§, Steven S. Rosenfeld{dagger},{ddagger}, and Peter Canoll§

Departments of {dagger}Neurology, {ddagger}Neurosurgery, and §Cell Biology and Pathology, and the Herbert Irving Comprehensive Cancer Center, Columbia University College of Physicians and Surgeons, New York, NY 10032

Submitted March 26, 2008; Revised May 6, 2008; Accepted May 13, 2008
Monitoring Editor: Erika Holzbaur

InCytes from MBC

The ability of gliomas to invade the brain limits the efficacy of standard therapies. In this study, we have examined glioma migration in living brain tissue by using two novel in vivo model systems. Within the brain, glioma cells migrate like nontransformed, neural progenitor cells—extending a prominent leading cytoplasmic process followed by a burst of forward movement by the cell body that requires myosin II. In contrast, on a two-dimensional surface, glioma cells migrate more like fibroblasts, and they do not require myosin II to move. To explain this phenomenon, we studied glioma migration through a series of synthetic membranes with defined pore sizes. Our results demonstrate that the A and B isoforms of myosin II are specifically required when a glioma cell has to squeeze through pores smaller than its nuclear diameter. They support a model in which the neural progenitor-like mode of glioma invasion and the requirement for myosin II represent an adaptation needed to move within the brain, which has a submicrometer effective pore size. Furthermore, the absolute requirement for myosin II in brain invasion underscores the importance of this molecular motor as a potential target for new anti-invasive therapies to treat malignant brain tumors.

This article was published online ahead of print in MBC in Press (http://www.molbiolcell.org/cgi/doi/10.1091/mbc.E08-03-0319) on May 21, 2008.

* These authors contributed equally to this work.

Address correspondence to: Steven S. Rosenfeld (sr2327{at}columbia.edu)

Abbreviations used: ECM, extracellular matrix; GFP, green fluorescent protein; PDGF, platelet-derived growth factor; RLC, regulatory light chain.


Related articles in Mol. Biol. Cell:

InCytes from MBC, August 2008

Mol. Biol. Cell 2008 19: 3179. [PDF]  



This article has been cited by other articles:


Home page
 Biophys. JHome page
B. M. Rubenstein and L. J. Kaufman
The Role of Extracellular Matrix in Glioma Invasion: A Cellular Potts Model Approach
Biophys. J., December 15, 2008; 95(12): 5661 - 5680.
[Abstract] [Full Text] [PDF]


Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
Copyright © 2008 by The American Society for Cell Biology. Terms of copyright protection, warranties, and disclaimers.