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Cell migration

cell migration, cell migration and invasion
Cell migration is a central process in the development and maintenance of multicellular organisms Tissue formation during embryonic development, wound healing and immune responses all require the orchestrated movement of cells in particular directions to specific locations Errors during this process have serious consequences, including intellectual disability, vascular disease, tumor formation and metastasis An understanding of the mechanism by which cells migrate may lead to the development of novel therapeutic strategies for controlling, for example, invasive tumour cells Cells often migrate in response to specific external signals, including chemical signals and mechanical signals

Due to the highly viscous environment low Reynolds number, cells need to permanently produce forces in order to move Cells achieve active movement by very different mechanisms Many less complex prokaryotic organisms and sperm cells use flagella or cilia to propel themselves Eukaryotic cell migration typically is far more complex and can consist of combinations of different migration mechanisms It generally involves drastic changes in cell shape which are driven by the cytoskeleton Two very distinct migration scenarios are crawling motion most commonly studied and blebbing motility


  • 1 Cell migration studies
    • 11 Common features
  • 2 Molecular processes of migration
    • 21 Cytoskeletal model A
    • 22 Leading Edge
    • 23 Trailing edge
    • 24 Membrane flow model B
    • 25 Collective biomechanical and molecular mechanism of cell motion
  • 3 Polarity in migrating cells
  • 4 Inverse problems in the context of cell motility
  • 5 See also
  • 6 External links
  • 7 References

Cell migration studies

Play media Figure 1: A Time-lapse microscopy video of migrating MCF-10A cells, imaged for 16 hours using quantitative phase microscopy

The migration of cultured cells attached to a surface is commonly studied using microscopy As cell movement is very slow, a few µm/minute, time-lapse microscopy videos are recorded of the migrating cells to speed up the movement Such videos Figure 1 reveal that the leading cell front is very active with a characteristic behavior of successive contractions and expansions It is generally accepted that the leading front is the main motor that pulls the cell forward

Common features

The processes underlying mammalian cell migration are believed to be consistent with those of non-spermatozooic locomotion Observations in common include:

  • cytoplasmic displacement at leading edge front
  • laminar removal of dorsally-accumulated debris toward trailing edge back

The latter feature is most easily observed when aggregates of a surface molecule are cross-linked with a fluorescent antibody or when small beads become artificially bound to the front of the cell

Other eukaryotic cells are observed to migrate similarly The amoeba Dictyostelium discoideum is useful to researchers because they consistently exhibit chemotaxis in response to cyclic AMP; they move more quickly than cultured mammalian cells; and they have a haploid genome that simplifies the process of connecting a particular gene product with its effect on cellular behaviour

Two different models for how cells move A Cytoskeletal model B Membrane Flow Model A Dynamic microtubules are necessary for tail retraction and are distributed at the rear end in a migrating cell Green, highly dynamic microtubules; yellow, moderately dynamic microtubules and red, stable microtubules B Stable microtubules act as struts and prevent tail retraction and thereby inhibit cell migration

Molecular processes of migration

There are two main theories for how the cell advances its front edge: the cytoskeletal model and membrane flow model It is possible that both underlying processes contribute to cell extension

Cytoskeletal model A

Leading Edge

Experimentation has shown that there is rapid actin polymerisation at the cell's front edge This observation has led to the hypothesis that formation of actin filaments "push" the leading edge forward and is the main motile force for advancing the cell’s front edge In addition, cytoskeletal elements are able to interact extensively and intimately with a cell's plasma membrane

Trailing edge

Other cytoskeletal components like microtubules have important functions in cell migration It has been found that microtubules act as “struts” that counteract the contractile forces that are needed for trailing edge retraction during cell movement When microtubules in the trailing edge of cell are dynamic, they are able to remodel to allow retraction When dynamics are suppressed, microtubules cannot remodel and, therefore, oppose the contractile forces The morphology of cells with suppressed microtubule dynamics indicate that cells can extended the front edge polarized in the direction of movement, but have difficulty retracting their trailing edge On the other hand high drug concentrations, or microtubule mutations that depolymerize the microtubules, can restore cell migration but there is a loss of directionality It can be concluded that microtubules act both to restrain cell movement and to establish directionality see "Polarity in Migrating Cells" below

Membrane flow model B

Studies have also shown that the front is the site at which membrane is returned to the cell surface from internal membrane pools at the end of the endocytic cycle This has led to the hypothesis that extension of the leading edge occurs primarily by addition of membrane at the front of the cell If so, the actin filaments that form at the front might stabilize the added membrane so that a structured extension, or lamella, is formed rather than a bubble-like structure or bleb at its front For a cell to move, it is necessary to bring a fresh supply of "feet" proteins called integrins, which attach a cell to the surface on which it is crawling to the front It is likely that these feet are endocytosed toward the rear of the cell and brought to the cell's front by exocytosis, to be reused to form new attachments to the substrate

Schematic representation of the collective biomechanical and molecular mechanism of cell motion

Collective biomechanical and molecular mechanism of cell motion

Based on some mathematical models, recent studies hypothesize a novel biological model for collective biomechanical and molecular mechanism of cell motion It is proposed that microdomains weave the texture of cytoskeleton and their interactions mark the location for formation of new adhesion sites According to this model, microdomain signaling dynamics organizes cytoskeleton and its interaction with substratum As microdomains trigger and maintain active polymerization of actin filaments, their propagation and zigzagging motion on the membrane generate a highly interlinked network of curved or linear filaments oriented at a wide spectrum of angles to the cell boundary It is also proposed that microdomain interaction marks the formation of new focal adhesion sites at the cell periphery Myosin interaction with the actin network then generate membrane retraction/ruffling, retrograde flow, and contractile forces for forward motion Finally, continuous application of stress on the old focal adhesion sites could result in the calcium-induced calpain activation, and consequently the detachment of focal adhesions which completes the cycle

Polarity in migrating cells

Migrating cells have a polarity—a front and a back Without it, they would move in all directions at once, ie spread How this polarity is formulated at a molecular level inside a cell is unknown In a cell that is meandering in a random way, the front can easily give way to become passive as some other region, or regions, of the cell forms a new front In chemotaxing cells, the stability of the front appears enhanced as the cell advances toward a higher concentration of the stimulating chemical This polarity is reflected at a molecular level by a restriction of certain molecules to particular regions of the inner cell surface Thus, the phospholipid PIP3 and activated Rac and CDC42 are found at the front of the cell, whereas Rho GTPase and PTEN are found toward the rear

It is believed that filamentous actins and microtubules are important for establishing and maintaining a cell’s polarity Drugs that destroy actin filaments have multiple and complex effects, reflecting the wide role that these filaments play in many cell processes It may be that, as part of the locomotory process, membrane vesicles are transported along these filaments to the cell’s front In chemotaxing cells, the increased persistence of migration toward the target may result from an increased stability of the arrangement of the filamentous structures inside the cell and determine its polarity In turn, these filamentous structures may be arranged inside the cell according to how molecules like PIP3 and PTEN are arranged on the inner cell membrane And where these are located appears in turn to be determined by the chemoattractant signals as these impinge on specific receptors on the cell’s outer surface

Although microtubules have been known to influence cell migration for many years, the mechanism by which they do so has remained controversial On a planar surface, microtubules are not needed for the movement, but they are required to provide directionality to cell movement and efficient protrusion of the leading edge When present, microtubules retard cell movement when their dynamics are suppressed by drug treatment or by tubulin mutations

Inverse problems in the context of cell motility

  • Inverse Problems

In a series of recent works a new area of research called inverse problems in cell motility has been established This approach is based on the idea that behavioral or shape changes of a cell bear information about the underlying mechanisms that generate these changes Reading cell motion, namely, understanding the underlying biophysical and mechanochemical processes, is of paramount importance The mathematical models developed in these works determine some physical features and material properties of the cells locally through analysis of live cell image sequences and uses this information to make further inferences about the molecular structures, dynamics, and processes within the cells, such as the actin network, microdomains, chemotaxis, adhesion, and retrograde flow

See also

  • Molecular and cellular biology portal
  • Cap formation
  • Chemotaxis
  • Durotaxis
  • Endocytic cycle
  • Neurophilia
  • Mouse models of breast cancer metastasis

External links

  • Cell Migration Gateway The Cell Migration Gateway is a comprehensive and regularly updated resource on cell migration
  • The Cytoskeleton and Cell Migration A tour of images and videos by the J V Small lab in Salzburg and Vienna
  • Time-lapse microscopy videos showing proliferating and migrating cells
  • Cell migration tracking by Phase Holographic Imaging AB


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  2. ^ Huber, F; Schnauss, J; Roenicke, S; Rauch, P; Mueller, K; Fuetterer, C; Kaes, J 2013 "Emergent complexity of the cytoskeleton: from single filaments to tissue" Advances in Physics 62 1: 1–112 doi:101080/000187322013771509 PMID 24748680  online
  3. ^ "HoloMonitor - Non-invasive image cytometers" Phase Holographic Imaging AB 
  4. ^ "What is Cell Migration" Cell Migration Gateway Cell MIgration Consortium Retrieved 24 March 2013 
  5. ^ Abercrombie, M; Heaysman, JE; Pegrum, SM 1970 "The locomotion of fibroblasts in culture III Movements of particles on the dorsal surface of the leading lamella" Experimental Cell Research 62 2: 389–98 doi:101016/0014-48277090570-7 PMID 5531377 
  6. ^ Wang, Y L 1985 "Exchange of actin subunits at the leading edge of living fibroblasts: possible role of treadmilling" The Journal of Cell Biology 101 2: 597–602 doi:101083/jcb1012597 PMC 2113673 PMID 4040521 
  7. ^ Mitchison, T; Cramer, LP 1996 "Actin-Based Cell Motility and Cell Locomotion" Cell 84 3: 371–9 doi:101016/S0092-86740081281-7 PMID 8608590 
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  9. ^ Doherty, Gary J; McMahon, Harvey T 2008 "Mediation, Modulation, and Consequences of Membrane-Cytoskeleton Interactions" Annual Review of Biophysics 37: 65–95 doi:101146/annurevbiophys37032807125912 PMID 18573073 
  10. ^ Yang, Hailing; Ganguly, Anutosh; Cabral, Fernando 2010 "Inhibition of Cell Migration and Cell Division Correlates with Distinct Effects of Microtubule Inhibiting Drugs" The Journal of Biological Chemistry 285 42: 32242–50 doi:101074/jbcM110160820 PMC 2952225 PMID 20696757 
  11. ^ a b c Ganguly, A; Yang, H; Sharma, R; Patel, K; Cabral, F 2012 "The Role of Microtubules and Their Dynamics in Cell Migration" J Biol Chem 287 52: 43359–69 doi:101074/jbcM112423905 PMID 23135278 
  12. ^ Bretscher, M S 1983 "Distribution of receptors for transferrin and low density lipoprotein on the surface of giant HeLa cells" Proceedings of the National Academy of Sciences 80 2: 454–8 doi:101073/pnas802454 PMC 393396 PMID 6300844 
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  17. ^ Meyer, AS; Hughes-Alford, SK; Kay, JE; Castillo, A; Wells, A; Gertler, FB; Lauffenburger, DA 2012 "2D protrusion but not motility predicts growth factor–induced cancer cell migration in 3D collagen" J Cell Biol 194 6: 721–729 doi:101083/jcb201201003 PMC 3373410 PMID 22665521 
  18. ^ Coskun, Huseyin 2006 Mathematical Models for Ameboid Cell Motility and Model Based Inverse Problems ProQuest 
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  20. ^ "Profiling Cells with Math" Mathematical Association of America 
  21. ^ "Mathematicians use cell 'profiling' to detect abnormalities -- including cancer" ScienceDaily 

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