Dimensions in cell migration

Doyle, Andrew D.; Petrie, Ryan J.; Kutys, Matthew L.; Yamada, Kenneth M.

doi:10.1016/j.ceb.2013.06.004

Cited by 170 publications

(156 citation statements)

References 64 publications

(67 reference statements)

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“…2,3 While some aspects of cell migration on 2D substrates are recapitulated in 3D environments, the specific mechanisms and regulation of migration can be dependent on the dimensionality of the matrix. 4 Indeed, recent studies with 3D cell culture models, which more closely mimic the microenvironment of tissues, have identified differences in cell morphology and modes of migration when compared with cell migration on 2D substrates. [5][6][7][8] For example, cells migrating in 3D matrices typically adopt a more elongated morphology and extend dendritic-like protrusions instead of the broad lamellipodia observed with cells migrating on 2D substrates.…”

Section: Introductionmentioning

confidence: 99%

The Rho family GEF Asef2 regulates cell migration in three dimensional (3D) collagen matrices through myosin II

Jean

Yang

Majumdar

et al. 2014

Cell Adhesion & Migration

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Cell migration is fundamental to a variety of physiological processes, including tissue development, homeostasis, and regeneration. Migration has been extensively studied with cells on 2-dimensional (2D) substrates, but much less is known about cell migration in 3D environments. Tissues and organs are 3D, which is the native environment of cells in vivo, pointing to a need to understand migration and the mechanisms that regulate it in 3D environments. To investigate cell migration in 3D environments, we developed microfluidic devices that afford a controlled, reproducible platform for generating 3D matrices. Using these devices, we show that the Rho family guanine nucleotide exchange factor (GEF) Asef2 inhibits cell migration in 3D type I collagen (collagen I) matrices. Treatment of cells with the myosin II (MyoII) inhibitor blebbistatin abolished the decrease in migration by Asef2. Moreover, Asef2 enhanced MyoII activity as shown by increased phosphorylation of serine 19 (S19). Furthermore, Asef2 increased activation of Rac, which is a Rho family small GTPase, in 3D collagen I matrices. Inhibition of Rac activity by treatment with the Rac-specific inhibitor NSC23766 abrogated the Asef2-promoted increase in S19 MyoII phosphorylation. Thus, our results indicate that Asef2 regulates cell migration in 3D collagen I matrices through a Rac-MyoII-dependent mechanism.

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Section: Introductionmentioning

confidence: 99%

The Rho family GEF Asef2 regulates cell migration in three dimensional (3D) collagen matrices through myosin II

Jean

Yang

Majumdar

et al. 2014

Cell Adhesion & Migration

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“…A number of studies demonstrated that cell migration in 2D may not reflect cell behaviors in more physiological relevant 3D models, where cells can be exposed to tissue-like confinement [25][26][27] and reciprocal cell-matrix interactions 28 One such model is the acid-soluble collagen gel, which provides fibrillar structure resembling the topography of tissue ECM, and therefore, is superior to the homogeneous 3D gels. 29 In 3D collagen gels with pore size equal to or larger than the diameter of cell nucleus, breast cancer cells utilize MMP-independent migration.…”

Section: Directed But Not Random Migration Of Cancer Cells In 3d Ismentioning

confidence: 99%

Directed, but not random, breast cancer cell migration is faster in the G1 phase of the cell cycle in 2D and 3D environments

et al. 2018

Preprint

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Cancer cell migration is essential for the early steps of metastasis, during which cancer cells move through the primary tumor and reach the blood vessels. In vivo, cancer cells are exposed to directional guidance cues, either soluble, such as gradients of growth factors, or insoluble, such as collagen fiber alignment. Depending on the number and strength of such cues, cells will migrate in a random or directed manner. Interestingly, similar cues also stimulate cell proliferation. In this regard, it is not clear whether cell cycle progression affects migration of cancer cells and whether this effect is different in random versus directed migration. In this study, we tested the effect of cell cycle progression on random and directed migration, both in 2D and 3D environments, in the breast carcinoma cell line, FUCCI-MDA-MB-231, using computational image analysis by LEVER. Directed migration in 2D was modeled as chemotaxis along a gradient of soluble EGF inside 10 µm-wide microchannels. In 3D, directed migration was modeled as contact guidance (alignotaxis) along aligned collagen fibers. Time-lapse recordings of cells in 2D and 3D revealed that directed, but not random migration, is cell cycle-dependent. In both 2D and 3D directed migration, cells in the G1 phase of the cell cycle outperformed cells in the G2 phase in terms of migration persistence and instantaneous velocity. These data suggest that in the presence of guidance cues in vivo, breast carcinoma cells in the G1 phase of the cell cycle may be more efficient in reaching vasculature.not peer-reviewed)

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“…A non-mutually exclusive possibility is that N-cad at the chain front interacts with axonal N-cad. Finally, the extracellular matrix (ECM) constitutes another key player in cell migration and interacts with cadherins (for reviews, see Doyle et al, 2013;Weber et al, 2011). Also, integrins in glia have been recently shown to shape the larval Drosophila CNS (Meyer et al, 2014).…”

Section: Cadherins and Ajsmentioning

confidence: 99%

N-cadherin negatively regulates collective Drosophila glial migration via actin cytoskeleton remodeling

Kumar

Gupta

Berzsenyi

et al. 2015

Journal of Cell Science

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Cell migration is an essential and highly regulated process. During development, glia cells and neurons migrate over long distancesin most cases collectively -to reach their final destination and build the sophisticated architecture of the nervous system, the most complex tissue of the body. Collective migration is highly stereotyped and efficient, defects in the process leading to severe human diseases that include mental retardation. This dynamic process entails extensive cell communication and coordination, hence, the real challenge is to analyze it in the entire organism and at cellular resolution. We here investigate the impact of the Ncadherin adhesion molecule on collective glial migration, by using the Drosophila developing wing and cell-type specific manipulation of gene expression. We show that N-cadherin timely accumulates in glial cells and that its levels affect migration efficiency. N-cadherin works as a molecular brake in a dosage-dependent manner, by negatively controlling actin nucleation and cytoskeleton remodeling through a/b catenins. This is the first in vivo evidence for N-cadherin negatively and cell autonomously controlling collective migration.

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Dimensions in cell migration

Cited by 170 publications

References 64 publications

The Rho family GEF Asef2 regulates cell migration in three dimensional (3D) collagen matrices through myosin II

The Rho family GEF Asef2 regulates cell migration in three dimensional (3D) collagen matrices through myosin II

Directed, but not random, breast cancer cell migration is faster in the G1 phase of the cell cycle in 2D and 3D environments

N-cadherin negatively regulates collective Drosophila glial migration via actin cytoskeleton remodeling

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