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Open AccessJournal ArticleDOI

Cell motility through plasma membrane blebbing

Oliver T. Fackler, +1 more
- 16 Jun 2008 - 
- Vol. 181, Iss: 6, pp 879-884
TLDR
It is proposed that in a physiological context, bleb-associated cell motility reflects a cell's response to reduced substratum adhesion and the importance of blebbing as a functional protrusion is underscores by the existence of multiple molecular mechanisms that govern actin-mediated bleb retraction.
Abstract
Plasma membrane blebs are dynamic cytoskeleton-regulated cell protrusions that have been implicated in apoptosis, cytokinesis, and cell movement. Influencing Rho–guanosine triphosphatase activities and subsequent actomyosin dynamics appears to constitute a core component for bleb formation. In this paper, we discuss recent evidence in support of a central role of nonapoptotic membrane blebbing for cell migration and cancer cell invasion as well as advances in our understanding of the underlying molecular mechanisms. Based on these studies, we propose that in a physiological context, bleb-associated cell motility reflects a cell's response to reduced substratum adhesion. The importance of blebbing as a functional protrusion is underscored by the existence of multiple molecular mechanisms that govern actin-mediated bleb retraction.

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Citations
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Cancer Invasion and the Microenvironment: Plasticity and Reciprocity

TL;DR: The cell-matrix and cell-cell adhesion, protease, and cytokine systems that underlie tissue invasion by cancer cells are described and explained to explain how the reciprocal reprogramming of both the tumor cells and the surrounding tissue structures not only guides invasion, but also generates diverse modes of dissemination.
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Plasticity of cell migration: a multiscale tuning model

TL;DR: Using a multiparameter tuning model, this work describes how dimension, density, stiffness, and orientation of the extracellular matrix together with cell determinants—including cell–cell and cell–matrix adhesion, cytoskeletal polarity and stiffness, etc.—interdependently control migration mode and efficiency.
Journal ArticleDOI

Random versus directionally persistent cell migration.

TL;DR: Factors such as the topography of the extracellular matrix, the cellular polarity machinery, receptor signalling, integrin trafficking, Integrin co-receptors and actomyosin contraction converge on regulation of the Rho family of GTPases and the control of lamellipodial protrusions to promote directional migration.
Journal ArticleDOI

Life at the Leading Edge

TL;DR: Four distinct protrusion methods likely act in concert to move cells through complex environments in vivo and require the coordination of a wide spectrum of signaling molecules and regulators of cytoskeletal dynamics.
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In vitro cell migration and invasion assays.

TL;DR: A concise summary of established migration/invasion assays described in the literature is provided, list advantages, limitations and drawbacks, give a tabular overview for convenience and depict the basic principles of the assays graphically.
References
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Journal ArticleDOI

Compensation mechanism in tumor cell migration: mesenchymal–amoeboid transition after blocking of pericellular proteolysis

TL;DR: The transition from proteolytic mesenchymal toward nonproteolytic amoeboid movement highlights a supramolecular plasticity mechanism in cell migration and further represents a putative escape mechanism in tumor cell dissemination after abrogation of pericellular proteolysis.
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Membrane blebbing during apoptosis results from caspase-mediated activation of ROCK I

TL;DR: It is shown that the Rho effector protein ROCK I, which contributes to phosphorylation of myosin light-chains, myOSin ATPase activity and coupling of actin–myosin filaments to the plasma membrane, is cleaved during apoptosis to generate a truncated active form.
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Differing modes of tumour cell invasion have distinct requirements for Rho/ROCK signalling and extracellular proteolysis

TL;DR: Two modes of tumour-cell motility in 3D matrices that involve different usage of Rho signalling are identified and combined blockade of extracellular proteases and ROCK negates the ability of tumours to switch between modes of motility and synergises to prevent tumour cell invasion.
Journal ArticleDOI

Rac Downregulates Rho Activity: Reciprocal Balance between Both Gtpases Determines Cellular Morphology and Migratory Behavior

TL;DR: It is concluded that Rac signaling is able to antagonize Rho activity directly at the GTPase level, and that the reciprocal balance between Rac and Rhoactivity determines cellular morphology and migratory behavior in NIH3T3 fibroblasts.
Journal ArticleDOI

Caspase-3-mediated cleavage of ROCK I induces MLC phosphorylation and apoptotic membrane blebbing

TL;DR: Activation of ROCK I by caspase-3 seems to be responsible for bleb formation in apoptotic cells.
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