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Journal articles on the topic 'Amoeboid motility'

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Author: Grafiati

Published: 14 March 2023

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1

Leo, Angela, Erica Pranzini, Laura Pietrovito, Elisa Pardella, Matteo Parri, Paolo Cirri, Gennaro Bruno, et al. "Claisened Hexafluoro Inhibits Metastatic Spreading of Amoeboid Melanoma Cells." Cancers 13, no. 14 (July 15, 2021): 3551. http://dx.doi.org/10.3390/cancers13143551.

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Metastatic melanoma is characterized by poor prognosis and a low free-survival rate. Thanks to their high plasticity, melanoma cells are able to migrate exploiting different cell motility strategies, such as the rounded/amoeboid-type motility and the elongated/mesenchymal-type motility. In particular, the amoeboid motility strongly contributes to the dissemination of highly invasive melanoma cells and no treatment targeting this process is currently available for clinical application. Here, we tested Claisened Hexafluoro as a novel inhibitor of the amoeboid motility. Reported data demonstrate that Claisened Hexafluoro specifically inhibits melanoma cells moving through amoeboid motility by deregulating mitochondrial activity and activating the AMPK signaling. Moreover, Claisened Hexafluoro is able to interfere with the adhesion abilities and the stemness features of melanoma cells, thus decreasing the in vivo metastatic process. This evidence may contribute to pave the way for future possible therapeutic applications of Claisened Hexafluoro to counteract metastatic melanoma dissemination.

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2

Pietrovito, Laura, Giuseppina Comito, Matteo Parri, Elisa Giannoni, Paola Chiarugi, and Maria Letizia Taddei. "Zoledronic Acid Inhibits the RhoA-mediated Amoeboid Motility of Prostate Cancer Cells." Current Cancer Drug Targets 19, no. 10 (December 23, 2019): 807–16. http://dx.doi.org/10.2174/1568009619666190115142858.

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Background:The bisphosphonate Zoledronic acid (ZA) is a potent osteoclast inhibitor currently used in the clinic to reduce osteoporosis and cancer-induced osteolysis. Moreover, ZA exerts an anti-tumor effect in several tumors. Despite this evidence, the relevance of ZA in prostate cancer (PCa) is not completely understood.Objective:To investigate the effect of ZA administration on the invasive properties of PC3 cells, which are characterised by RhoA-dependent amoeboid motility.Methods:The effect of ZA administration on the in vitro invasive properties of PC3 cells was evaluated by cell migration in 3D collagen matrices, immunofluorescence and Boyden assays or transendothelial migration. Lung retention and colonization assays were performed to assess the efficacy of ZA administration in vivo.Results:PC3 cells are characterised by RhoA-dependent amoeboid motility. We now report a clear inhibition of in vitro PC3 cell invasion and RhoA activity upon ZA treatment. Moreover, to confirm a specific role of ZA in the inhibition of amoeboid motility of PC3 cells, we demonstrate that ZA interferes only partially with PC3 cells showing a mesenchymal phenotype due to both treatment with conditioned medium of cancer associated fibroblasts or to the acquisition of chemoresistance. Furthermore, we demonstrate that ZA impairs adhesion to endothelial cells and the trans-endothelial cell migration, two essential properties characterising amoeboid motility and PC3 metastatic dissemination. In vivo experiments prove the ability of ZA to inhibit the metastatic process of PC3 cells as shown by the decrease in lung colonization.Conclusion:This study demonstrates that ZA inhibits Rho-dependent amoeboid motility of PC3 cells, thus suggesting ZA as a potential therapy to impede the metastatic dissemination of PC3 cells.

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3

Klemm, Lucas C., Ryan A. Denu, Laurel E. Hind, Briana L. Rocha-Gregg, Mark E. Burkard, and Anna Huttenlocher. "Centriole and Golgi microtubule nucleation are dispensable for the migration of human neutrophil-like cells." Molecular Biology of the Cell 32, no. 17 (August 15, 2021): 1545–56. http://dx.doi.org/10.1091/mbc.e21-02-0060.

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4

Callan-Jones, A. C., and R. Voituriez. "Active gel model of amoeboid cell motility." New Journal of Physics 15, no. 2 (February 18, 2013): 025022. http://dx.doi.org/10.1088/1367-2630/15/2/025022.

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5

Peretz-Soroka, Hagit, Reuven Tirosh, Jolly Hipolito, Erwin Huebner, Murray Alexander, Jason Fiege, and Francis Lin. "A bioenergetic mechanism for amoeboid-like cell motility profiles tested in a microfluidic electrotaxis assay." Integrative Biology 9, no. 11 (2017): 844–56. http://dx.doi.org/10.1039/c7ib00086c.

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6

Dalal, Swapnil, Alexander Farutin, and Chaouqi Misbah. "Amoeboid swimming in a compliant channel." Soft Matter 16, no. 6 (2020): 1599–613. http://dx.doi.org/10.1039/c9sm01689a.

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We studied influence of elasticity of surrounding environment on cell motility by numerically investigating effects of wall flexibility and channel confinement on flow dynamics of amoeboid swimming in compliant channel.

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7

Saito, Koji, Yuta Ozawa, Keisuke Hibino, and Yasutaka Ohta. "FilGAP, a Rho/Rho-associated protein kinase–regulated GTPase-activating protein for Rac, controls tumor cell migration." Molecular Biology of the Cell 23, no. 24 (December 15, 2012): 4739–50. http://dx.doi.org/10.1091/mbc.e12-04-0310.

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Tumor cells exhibit two interconvertible modes of cell motility referred to as mesenchymal and amoeboid migration. Mesenchymal mode is characterized by elongated morphology that requires high GTPase Rac activation, whereas amoeboid mode is dependent on actomyosin contractility induced by Rho/Rho-associated protein kinase (ROCK) signaling. While elongated morphology is driven by Rac-induced protrusion at the leading edge, how Rho/ROCK signaling controls amoeboid movement is not well understood. We identified FilGAP, a Rac GTPase-activating protein (GAP), as a mediator of Rho/ROCK-dependent amoeboid movement of carcinoma cells. We show that depletion of endogenous FilGAP in carcinoma cells induced highly elongated mesenchymal morphology. Conversely, forced expression of FilGAP induced a round/amoeboid morphology that requires Rho/ROCK-dependent phosphorylation of FilGAP. Moreover, depletion of FilGAP impaired breast cancer cell invasion through extracellular matrices and reduced tumor cell extravasation in vivo. Thus phosphorylation of FilGAP by ROCK appears to promote amoeboid morphology of carcinoma cells, and FilGAP contributes to tumor invasion.

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8

Copos, Calina A., Robert D. Guy, Sam Walcott, Juan Carlos del Alamo, and Alex Mogilner. "Mechanosensitive Adhesion Explains Stepping Motility in Amoeboid Cells." Biophysical Journal 112, no. 3 (February 2017): 433a. http://dx.doi.org/10.1016/j.bpj.2016.11.2315.

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9

Bullock, Timothy L., Airlie J. McCoy, Helen M. Kent, Thomas M. Roberts, and Murray Stewart. "Structural basis for amoeboid motility in nematode sperm." Nature Structural Biology 5, no. 3 (March 1998): 184–89. http://dx.doi.org/10.1038/nsb0398-184.

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10

Copos, Calina A., Sam Walcott, Juan C. del Álamo, Effie Bastounis, Alex Mogilner, and Robert D. Guy. "Mechanosensitive Adhesion Explains Stepping Motility in Amoeboid Cells." Biophysical Journal 112, no. 12 (June 2017): 2672–82. http://dx.doi.org/10.1016/j.bpj.2017.04.033.

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11

Titus, Margaret A., and Holly V. Goodson. "An evolutionary perspective on cell migration: Digging for the roots of amoeboid motility." Journal of Cell Biology 216, no. 6 (May 24, 2017): 1509–11. http://dx.doi.org/10.1083/jcb.201704112.

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Fritz-Laylin et al. (2017. J. Cell Biol. https://doi.org/10.1083/jcb.201701074) take advantage of the deep knowledge of mechanisms of actin-based motility and a growing number of sequenced genomes across the tree of life to gain insight into the machinery needed for pseudopod-based amoeboid motility and how it evolved.

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12

Peretz-Soroka, Hagit, Reuven Tirosh, Jolly Hipolito, Erwin Huebner, Murray Alexander, Jason Fiege, and Francis Lin. "Correction: A bioenergetic mechanism for amoeboid-like cell motility profiles tested in a microfluidic electrotaxis assay." Integrative Biology 9, no. 11 (2017): 892–93. http://dx.doi.org/10.1039/c7ib90031g.

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Correction for ‘A bioenergetic mechanism for amoeboid-like cell motility profiles tested in a microfluidic electrotaxis assay’ by Hagit Peretz-Soroka et al., Integr. Biol., 2017, DOI: 10.1039/c7ib00086c.

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13

Bastounis, Effie, Ruedi Meili, Begoña Álvarez-González, Joshua Francois, Juan C. del Álamo, Richard A. Firtel, and Juan C. Lasheras. "Both contractile axial and lateral traction force dynamics drive amoeboid cell motility." Journal of Cell Biology 204, no. 6 (March 17, 2014): 1045–61. http://dx.doi.org/10.1083/jcb.201307106.

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Chemotaxing Dictyostelium discoideum cells adapt their morphology and migration speed in response to intrinsic and extrinsic cues. Using Fourier traction force microscopy, we measured the spatiotemporal evolution of shape and traction stresses and constructed traction tension kymographs to analyze cell motility as a function of the dynamics of the cell’s mechanically active traction adhesions. We show that wild-type cells migrate in a step-wise fashion, mainly forming stationary traction adhesions along their anterior–posterior axes and exerting strong contractile axial forces. We demonstrate that lateral forces are also important for motility, especially for migration on highly adhesive substrates. Analysis of two mutant strains lacking distinct actin cross-linkers (mhcA− and abp120− cells) on normal and highly adhesive substrates supports a key role for lateral contractions in amoeboid cell motility, whereas the differences in their traction adhesion dynamics suggest that these two strains use distinct mechanisms to achieve migration. Finally, we provide evidence that the above patterns of migration may be conserved in mammalian amoeboid cells.

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14

Campbell, Eric J., and Prosenjit Bagchi. "A computational model of amoeboid cell motility in the presence of obstacles." Soft Matter 14, no. 28 (2018): 5741–63. http://dx.doi.org/10.1039/c8sm00457a.

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15

Lees, J. G., C. T. T. Bach, P. Bradbury, A. Paul, P. W. Gunning, and G. M. O'Neill. "The actin-associating protein Tm5NM1 blocks mesenchymal motility without transition to amoeboid motility." Oncogene 30, no. 10 (November 15, 2010): 1241–51. http://dx.doi.org/10.1038/onc.2010.516.

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16

Berton, Stefania, Barbara Belletti, Katarina Wolf, Vincenzo Canzonieri, Francesca Lovat, Andrea Vecchione, Alfonso Colombatti, Peter Friedl, and Gustavo Baldassarre. "The Tumor Suppressor Functions of p27kip1 Include Control of the Mesenchymal/Amoeboid Transition." Molecular and Cellular Biology 29, no. 18 (July 13, 2009): 5031–45. http://dx.doi.org/10.1128/mcb.00144-09.

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ABSTRACT In many human cancers, p27 downregulation correlates with a worse prognosis, suggesting that p27 levels could represent an important determinant in cell transformation and cancer development. Using a mouse model system based on v-src-induced transformation, we show here that p27 absence is always linked to a more aggressive phenotype. When cultured in three-dimensional contexts, v-src-transformed p27-null fibroblasts undergo a morphological switch from an elongated to a rounded cell shape, accompanied by amoeboid-like morphology and motility. Importantly, the acquisition of the amoeboid motility is associated with a greater ability to move and colonize distant sites in vivo. The reintroduction of different p27 mutants in v-src-transformed p27-null cells demonstrates that the control of cell proliferation and motility represents two distinct functions of p27, both necessary for it to fully act as a tumor suppressor. Thus, we highlight here a new p27 function in driving cell plasticity that is associated with its C-terminal portion and does not depend on the control of cyclin-dependent kinase activity.

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17

SHIMABUKURO, Katsuya. "Reconstitution of MSP-Based Amoeboid Motility Using Ascaris Sperm." Seibutsu Butsuri 53, no. 5 (2013): 266–67. http://dx.doi.org/10.2142/biophys.53.266.

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18

Miao, Long, Orion Vanderlinde, Murray Stewart, and Thomas M. Roberts. "Retraction in Amoeboid Cell Motility Powered by Cytoskeletal Dynamics." Science 302, no. 5649 (November 20, 2003): 1405–7. http://dx.doi.org/10.1126/science.1089129.

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19

Bastounis, Effie, Begoña Álvarez-González, Juan C. del Álamo, Juan C. Lasheras, and Richard A. Firtel. "Cooperative cell motility during tandem locomotion of amoeboid cells." Molecular Biology of the Cell 27, no. 8 (April 15, 2016): 1262–71. http://dx.doi.org/10.1091/mbc.e15-12-0836.

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Streams of migratory cells are initiated by the formation of tandem pairs of cells connected head to tail to which other cells subsequently adhere. The mechanisms regulating the transition from single to streaming cell migration remain elusive, although several molecules have been suggested to be involved. In this work, we investigate the mechanics of the locomotion of Dictyostelium tandem pairs by analyzing the spatiotemporal evolution of their traction adhesions (TAs). We find that in migrating wild-type tandem pairs, each cell exerts traction forces on stationary sites (∼80% of the time), and the trailing cell reuses the location of the TAs of the leading cell. Both leading and trailing cells form contractile dipoles and synchronize the formation of new frontal TAs with ∼54-s time delay. Cells not expressing the lectin discoidin I or moving on discoidin I–coated substrata form fewer tandems, but the trailing cell still reuses the locations of the TAs of the leading cell, suggesting that discoidin I is not responsible for a possible chemically driven synchronization process. The migration dynamics of the tandems indicate that their TAs’ reuse results from the mechanical synchronization of the leading and trailing cells’ protrusions and retractions (motility cycles) aided by the cell–cell adhesions.

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20

Bottino, Dean, Alexander Mogilner, Tom Roberts, Murray Stewart, and George Oster. "How nematode sperm crawl." Journal of Cell Science 115, no. 2 (January 15, 2002): 367–84. http://dx.doi.org/10.1242/jcs.115.2.367.

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Sperm of the nematode, Ascaris suum, crawl using lamellipodial protrusion, adhesion and retraction, a process analogous to the amoeboid motility of other eukaryotic cells. However, rather than employing an actin cytoskeleton to generate locomotion, nematode sperm use the major sperm protein (MSP). Moreover, nematode sperm lack detectable molecular motors or the battery of actin-binding proteins that characterize actin-based motility. The Ascaris system provides a simple ‘stripped down’ version of a crawling cell in which to examine the basic mechanism of cell locomotion independently of other cellular functions that involve the cytoskeleton. Here we present a mechanochemical analysis of crawling in Ascaris sperm. We construct a finite element model wherein (a) localized filament polymerization and bundling generate the force for lamellipodial extension and (b) energy stored in the gel formed from the filament bundles at the leading edge is subsequently used to produce the contraction that pulls the rear of the cell forward. The model reproduces the major features of crawling sperm and provides a framework in which amoeboid cell motility can be analyzed. Although the model refers primarily to the locomotion of nematode sperm, it has important implications for the mechanics of actin-based cell motility.Movies available on-line.

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21

Zhu, Xiaoying, Roland Bouffanais, and Dick K. P. Yue. "Interplay between motility and cell-substratum adhesion in amoeboid cells." Biomicrofluidics 9, no. 5 (September 2015): 054112. http://dx.doi.org/10.1063/1.4931762.

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22

Jones, Brandon C., Laura C. Kelley, Yuriy V. Loskutov, Kristina M. Marinak, Varvara K. Kozyreva, Matthew B. Smolkin, and Elena N. Pugacheva. "Dual Targeting of Mesenchymal and Amoeboid Motility Hinders Metastatic Behavior." Molecular Cancer Research 15, no. 6 (February 24, 2017): 670–82. http://dx.doi.org/10.1158/1541-7786.mcr-16-0411.

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23

Laser-Azogui, A., T. Diamant-Levi, S. Israeli, Y. Roytman, and I. Tsarfaty. "Met-induced membrane blebbing leads to amoeboid cell motility and invasion." Oncogene 33, no. 14 (May 13, 2013): 1788–98. http://dx.doi.org/10.1038/onc.2013.138.

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24

Xiong, Yuan, Cathryn Kabacoff, Jonathan Franca-Koh, Peter N. Devreotes, Douglas N. Robinson, and Pablo A. Iglesias. "Automated characterization of cell shape changes during amoeboid motility by skeletonization." BMC Systems Biology 4, no. 1 (2010): 33. http://dx.doi.org/10.1186/1752-0509-4-33.

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25

Kitzing, T. M., Y. Wang, O. Pertz, J. W. Copeland, and R. Grosse. "Formin-like 2 drives amoeboid invasive cell motility downstream of RhoC." Oncogene 29, no. 16 (January 25, 2010): 2441–48. http://dx.doi.org/10.1038/onc.2009.515.

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26

Miao, L., O. Vanderlinde, J. Liu, R. P. Grant, A. Wouterse, K. Shimabukuro, A. Philipse, M. Stewart, and T. M. Roberts. "The role of filament-packing dynamics in powering amoeboid cell motility." Proceedings of the National Academy of Sciences 105, no. 14 (April 2, 2008): 5390–95. http://dx.doi.org/10.1073/pnas.0708416105.

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27

Ruprecht, Verena, Stefan Wieser, Andrew Callan-Jones, Michael Smutny, Hitoshi Morita, Keisuke Sako, Vanessa Barone, et al. "Cortical Contractility Triggers a Stochastic Switch to Fast Amoeboid Cell Motility." Cell 160, no. 4 (February 2015): 673–85. http://dx.doi.org/10.1016/j.cell.2015.01.008.

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28

Schindler, Daniel, Ted Moldenhawer, Maike Stange, Valentino Lepro, Carsten Beta, Matthias Holschneider, and Wilhelm Huisinga. "Analysis of protrusion dynamics in amoeboid cell motility by means of regularized contour flows." PLOS Computational Biology 17, no. 8 (August 23, 2021): e1009268. http://dx.doi.org/10.1371/journal.pcbi.1009268.

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Amoeboid cell motility is essential for a wide range of biological processes including wound healing, embryonic morphogenesis, and cancer metastasis. It relies on complex dynamical patterns of cell shape changes that pose long-standing challenges to mathematical modeling and raise a need for automated and reproducible approaches to extract quantitative morphological features from image sequences. Here, we introduce a theoretical framework and a computational method for obtaining smooth representations of the spatiotemporal contour dynamics from stacks of segmented microscopy images. Based on a Gaussian process regression we propose a one-parameter family of regularized contour flows that allows us to continuously track reference points (virtual markers) between successive cell contours. We use this approach to define a coordinate system on the moving cell boundary and to represent different local geometric quantities in this frame of reference. In particular, we introduce the local marker dispersion as a measure to identify localized membrane expansions and provide a fully automated way to extract the properties of such expansions, including their area and growth time. The methods are available as an open-source software package called AmoePy, a Python-based toolbox for analyzing amoeboid cell motility (based on time-lapse microscopy data), including a graphical user interface and detailed documentation. Due to the mathematical rigor of our framework, we envision it to be of use for the development of novel cell motility models. We mainly use experimental data of the social amoeba Dictyostelium discoideum to illustrate and validate our approach.

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29

King, K. L., M. Stewart, T. M. Roberts, and M. Seavy. "Structure and macromolecular assembly of two isoforms of the major sperm protein (MSP) from the amoeboid sperm of the nematode, Ascaris suum." Journal of Cell Science 101, no. 4 (April 1, 1992): 847–57. http://dx.doi.org/10.1242/jcs.101.4.847.

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Ascaris sperm are amoeboid cells that crawl by extending pseudopods. Although amoeboid motility is generally mediated through an actin-based cytoskeleton, Ascaris sperm lack this system. Instead, their major sperm protein (MSP) forms an extensive filament system that appears to fulfil this function. Because their motility appears to be essentially the same as that of their actin-rich counterparts, Ascaris sperm offer a simple alternative system for investigation of the molecular mechanism of amoeboid movement. To examine the structure and composition of the cytoskeleton, we stabilized the extremely labile native MSP filaments by detergent lysis of sperm in the presence of either glutaraldehyde or polyethylene glycol (PEG). Biochemical analysis showed that the cytoskeleton contained two isoforms of MSP, designated alpha- and beta-, that we purified and sequenced. Both contain 126 amino acids and have an acetylated N-terminal alanine, but differ at four residues so that alpha-MSP is 142 Da larger and 0.6 pH unit more basic than beta-MSP. Neither isoform shares sequence homology with other cytoskeletal proteins. In ethanol, 2-methyl-2,4-pentanediol (MPD), and other water-miscible alcohols each isoform assembled into filaments 10 nm wide with a characteristic substructure repeating axially at 9 nm. These filaments were indistinguishable from native fibers isolated from detergent-lysed sperm. Pelleting assays indicated a critical concentration for assembly of 0.2 mM for both isoforms in 30% ethanol, but alpha-MSP formed filaments at lower solvent concentration than beta-MSP. When incubated in polyethylene glycol, both isoforms formed thin, needle-shaped crystals that appeared to be constructed from helical fibers, with a 9 nm axial repeat that matched that seen in isolated filaments. These crystals probably contained a parallel array of helical filaments, and may enable both the structure of MSP molecules and their mode of assembly into higher aggregates to be investigated to high resolution.

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30

Joos, Luc, and Claude Gicquaud. "Effect of phalloidin and viroisin on Acanthamoeba castellanii after permeabilization of the cell." Biochemistry and Cell Biology 65, no. 3 (March 1, 1987): 261–70. http://dx.doi.org/10.1139/o87-034.

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We have developed a new technique for the permeabilization of the membrane of Acanthamoeba castellanii. This technique involves the use of digitonin which alters neither the morphology nor the motility of the cell, but favours the penetration of phalloidin and viroisin. Treatment of permeabilized cells with phalloidin or viroisin induces, in the cortex of the cell, an intensive proliferation of filaments which have been identified as actin. This cortical filamentous layer detaches from the membrane and slowly contracts, acting as a fine mesh sieve which concentrates the organelles in the middle of the cell, causing therefore the formation of a central granuloplasm and a cortical hyaloplasm. During this process, cell motility is irreversibly lost. The results indicate that extensive proliferation and reorganization of actin filaments cannot support cell motility and they are discussed in terms of a general understanding of amoeboid movement.

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31

Arcizet, Delphine, Sofia Capito, Mari Gorelashvili, Carolin Leonhardt, Marion Vollmer, Simon Youssef, Susanne Rappl, and Doris Heinrich. "Contact-controlled amoeboid motility induces dynamic cell trapping in 3D-microstructured surfaces." Soft Matter 8, no. 5 (2012): 1473–81. http://dx.doi.org/10.1039/c1sm05615h.

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32

Ferling, Iuliia, Silvia Radosa, and Falk Hillmann. "Jäger und Gejagte — wie sich Pilze gegen räuberische Amöben wehren." BIOspektrum 27, no. 5 (September 2021): 469–72. http://dx.doi.org/10.1007/s12268-021-1617-1.

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AbstractWhat seems obvious for most free-living bacteria, also appeals for yeast and filamentous fungi: their natural reservoirs include a variety of micropredators, such as members of the Amoebozoa kingdom. Not only do they share a predatory lifestyle, but their amoeboid motility and way of ingesting living microbial food reveals several similarities to innate immune cells. Understanding how fungi have learned to cope with such environmental phagocytes will shed new light on the evolutionary driving forces of fungal diversity and virulence.

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Bastounis, Effie, Ruedi Meili, Baldomero Alonso-Latorre, Juan C. del Álamo, Juan C. Lasheras, and Richard A. Firtel. "The SCAR/WAVE complex is necessary for proper regulation of traction stresses during amoeboid motility." Molecular Biology of the Cell 22, no. 21 (November 2011): 3995–4003. http://dx.doi.org/10.1091/mbc.e11-03-0278.

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Cell migration requires a tightly regulated, spatiotemporal coordination of underlying biochemical pathways. Crucial to cell migration is SCAR/WAVE–mediated dendritic F-actin polymerization at the cell's leading edge. Our goal is to understand the role the SCAR/WAVE complex plays in the mechanics of amoeboid migration. To this aim, we measured and compared the traction stresses exerted by Dictyostelium cells lacking the SCAR/WAVE complex proteins PIR121 (pirA−) and SCAR (scrA−) with those of wild-type cells while they were migrating on flat, elastic substrates. We found that, compared to wild type, both mutant strains exert traction stresses of different strengths that correlate with their F-actin levels. In agreement with previous studies, we found that wild-type cells migrate by repeating a motility cycle in which the cell length and strain energy exerted by the cells on their substrate vary periodically. Our analysis also revealed that scrA− cells display an altered motility cycle with a longer period and a lower migration velocity, whereas pirA− cells migrate in a random manner without implementing a periodic cycle. We present detailed characterization of the traction-stress phenotypes of the various cell lines, providing new insights into the role of F-actin polymerization in regulating cell–substratum interactions and stresses required for motility.

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Belletti, Barbara, Ilenia Pellizzari, Stefania Berton, Linda Fabris, Katarina Wolf, Francesca Lovat, Monica Schiappacassi, et al. "p27kip1 Controls Cell Morphology and Motility by Regulating Microtubule-Dependent Lipid Raft Recycling." Molecular and Cellular Biology 30, no. 9 (March 1, 2010): 2229–40. http://dx.doi.org/10.1128/mcb.00723-09.

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ABSTRACT p27kip1 (p27) is an inhibitor of cyclin/cyclin-dependent kinase complexes, whose nuclear loss indicates a poor prognosis in various solid tumors. When located in the cytoplasm, p27 binds Op18/stathmin (stathmin), a microtubule (MT)-destabilizing protein, and restrains its activity. This leads to MT stabilization, which negatively affects cell migration. Here, we demonstrate that this p27 function also influences morphology and motility of cells immersed in three-dimensional (3D)matrices. Cells lacking p27 display a decrease in MT stability, a rounded shape when immersed in 3D environments, and a mesenchymal-amoeboid conversion in their motility mode. Upon cell contact to extracellular matrix, the decreased MT stability observed in p27 null cells results in accelerated lipid raft trafficking and increased RhoA activity. Importantly, cell morphology, motility, MT network composition, and distribution of p27 null cells were rescued by the concomitant genetic ablation of Stathmin, implicating that the balanced expression of p27 and stathmin represents a crucial determinant for cytoskeletal organization and cellular behavior in 3D contexts.

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35

Eisenmann, KM. "Regulation of Cortical Actin Cytoskeleton and Amoeboid Motility through the mDia2/DIP Complex." Microscopy and Microanalysis 16, S2 (July 2010): 1002–3. http://dx.doi.org/10.1017/s1431927610056631.

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36

Tooley, Aaron J., Julia Gilden, Jordan Jacobelli, Peter Beemiller, William S. Trimble, Makoto Kinoshita, and Matthew F. Krummel. "Amoeboid T lymphocytes require the septin cytoskeleton for cortical integrity and persistent motility." Nature Cell Biology 11, no. 1 (November 30, 2008): 17–26. http://dx.doi.org/10.1038/ncb1808.

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37

Rochelle, Tristan, Thomas Daubon, Marleen Van Troys, Thomas Harnois, Davy Waterschoot, Christophe Ampe, Lydia Roy, Nicolas Bourmeyster, and Bruno Constantin. "p210 bcr‐abl induces amoeboid motility by recruiting ADF/destrin through RhoA/ROCK1." FASEB Journal 27, no. 1 (October 9, 2012): 123–34. http://dx.doi.org/10.1096/fj.12-205112.

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Mills, Evan, and Kevin Truong. "Analysis and regulation of amoeboid-like cell motility using synthetic Ca2+-sensitive proteins." Cell Calcium 53, no. 3 (March 2013): 231–40. http://dx.doi.org/10.1016/j.ceca.2012.12.005.

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Rodriguez, Maria Antonia, Lawrence L. LeClaire, and Thomas M. Roberts. "Preparing to move: Assembly of the MSP amoeboid motility apparatus during spermiogenesis inAscaris." Cell Motility and the Cytoskeleton 60, no. 4 (2005): 191–99. http://dx.doi.org/10.1002/cm.20058.

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40

Ahn, J., V. Sanz-Moreno, and C. J. Marshall. "The metastasis gene NEDD9 product acts through integrin 3 and Src to promote mesenchymal motility and inhibit amoeboid motility." Journal of Cell Science 125, no. 7 (February 10, 2012): 1814–26. http://dx.doi.org/10.1242/jcs.101444.

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Beck, Thomas C., Ana Cordeiro Gomes, Jason G. Cyster, and João P. Pereira. "CXCR4 and a cell-extrinsic mechanism control immature B lymphocyte egress from bone marrow." Journal of Experimental Medicine 211, no. 13 (November 17, 2014): 2567–81. http://dx.doi.org/10.1084/jem.20140457.

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Leukocyte residence in lymphoid organs is controlled by a balance between retention and egress-promoting chemoattractants sensed by pertussis toxin (PTX)–sensitive Gαi protein–coupled receptors (GPCRs). Here, we use two-photon intravital microscopy to show that immature B cell retention within bone marrow (BM) was strictly dependent on amoeboid motility mediated by CXCR4 and CXCL12 and by α4β1 integrin–mediated adhesion to VCAM-1. However, B lineage cell egress from BM is independent of PTX-sensitive GPCR signaling. B lineage cells expressing PTX rapidly exited BM even though their motility within BM parenchyma was significantly reduced. Our experiments reveal that when immature B cells are near BM sinusoids their motility is reduced, their morphology is predominantly rounded, and cells reverse transmigrate across sinusoidal endothelium in a largely nonamoeboid manner. Immature B cell egress from BM was dependent on a twofold CXCR4 down-regulation that was antagonized by antigen-induced BCR signaling. This passive mode of cell egress from BM also contributes significantly to the export of other hematopoietic cells, including granulocytes, monocytes, and NK cells, and is reminiscent of erythrocyte egress.

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Belletti, Barbara, Milena S. Nicoloso, Monica Schiappacassi, Stefania Berton, Francesca Lovat, Katarina Wolf, Vincenzo Canzonieri, et al. "Stathmin Activity Influences Sarcoma Cell Shape, Motility, and Metastatic Potential." Molecular Biology of the Cell 19, no. 5 (May 2008): 2003–13. http://dx.doi.org/10.1091/mbc.e07-09-0894.

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The balanced activity of microtubule-stabilizing and -destabilizing proteins determines the extent of microtubule dynamics, which is implicated in many cellular processes, including adhesion, migration, and morphology. Among the destabilizing proteins, stathmin is overexpressed in different human malignancies and has been recently linked to the regulation of cell motility. The observation that stathmin was overexpressed in human recurrent and metastatic sarcomas prompted us to investigate stathmin contribution to tumor local invasiveness and distant dissemination. We found that stathmin stimulated cell motility in and through the extracellular matrix (ECM) in vitro and increased the metastatic potential of sarcoma cells in vivo. On contact with the ECM, stathmin was negatively regulated by phosphorylation. Accordingly, a less phosphorylable stathmin point mutant impaired ECM-induced microtubule stabilization and conferred a higher invasive potential, inducing a rounded cell shape coupled with amoeboid-like motility in three-dimensional matrices. Our results indicate that stathmin plays a significant role in tumor metastasis formation, a finding that could lead to exploitation of stathmin as a target of new antimetastatic drugs.

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Gilden, Julia K., Sebastian Peck, Yi-Chun M. Chen, and Matthew F. Krummel. "The septin cytoskeleton facilitates membrane retraction during motility and blebbing." Journal of Cell Biology 196, no. 1 (January 9, 2012): 103–14. http://dx.doi.org/10.1083/jcb.201105127.

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Increasing evidence supports a critical role for the septin cytoskeleton at the plasma membrane during physiological processes including motility, formation of dendritic spines or cilia, and phagocytosis. We sought to determine how septins regulate the plasma membrane, focusing on this cytoskeletal element’s role during effective amoeboid motility. Surprisingly, septins play a reactive rather than proactive role, as demonstrated during the response to increasing hydrostatic pressure and subsequent regulatory volume decrease. In these settings, septins were required for rapid cortical contraction, and SEPT6-GFP was recruited into filaments and circular patches during global cortical contraction and also specifically during actin filament depletion. Recruitment of septins was also evident during excessive blebbing initiated by blocking membrane trafficking with a dynamin inhibitor, providing further evidence that septins are recruited to facilitate retraction of membranes during dynamic shape change. This function of septins in assembling on an unstable cortex and retracting aberrantly protruding membranes explains the excessive blebbing and protrusion observed in septin-deficient T cells.

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Romanovskii, Yurii M., and V. A. Teplov. "The physical bases of cell movement. The mechanisms of self-organisation of amoeboid motility." Uspekhi Fizicheskih Nauk 165, no. 5 (1995): 555. http://dx.doi.org/10.3367/ufnr.0165.199505c.0555.

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Romanovskii, Yurii M., and V. A. Teplov. "The physical bases of cell movement. The mechanisms of self-organisation of amoeboid motility." Physics-Uspekhi 38, no. 5 (May 31, 1995): 521–42. http://dx.doi.org/10.1070/pu1995v038n05abeh000086.

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Taddei, Maria Letizia, Matteo Parri, Adriano Angelucci, Francesca Bianchini, Chiara Marconi, Elisa Giannoni, Giovanni Raugei, Mauro Bologna, Lido Calorini, and Paola Chiarugi. "EphA2 Induces Metastatic Growth Regulating Amoeboid Motility and Clonogenic Potential in Prostate Carcinoma Cells." Molecular Cancer Research 9, no. 2 (January 4, 2011): 149–60. http://dx.doi.org/10.1158/1541-7786.mcr-10-0298.

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TARFULEA, NICOLETA. "A DISCRETE MATHEMATICAL MODEL FOR SINGLE AND COLLECTIVE MOVEMENT IN AMOEBOID CELLS." Journal of Biological Systems 26, no. 02 (June 2018): 275–300. http://dx.doi.org/10.1142/s0218339018500134.

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In this paper, we develop a new discrete mathematical model for individual and collective cell motility. We introduce a mechanical model for the movement of a cell on a two-dimensional rigid surface to describe and investigate the cell–cell and cell–substrate interactions. The cell cytoskeleton is modeled as a series of springs and dashpots connected in parallel. The cell–substrate attachments and the cell protrusions are also included. In particular, this model is used to describe the directed movement of endothelial cells on a Matrigel plate. We compare the results from our model with experimental data. We show that cell density and substrate rigidity play an important role in network formation.

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Lewis, Owen L., Shun Zhang, Robert D. Guy, and Juan C. del Álamo. "Coordination of contractility, adhesion and flow in migrating Physarum amoebae." Journal of The Royal Society Interface 12, no. 106 (May 2015): 20141359. http://dx.doi.org/10.1098/rsif.2014.1359.

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This work examines the relationship between spatio-temporal coordination of intracellular flow and traction stress and the speed of amoeboid locomotion of microplasmodia of Physarum polycephalum . We simultaneously perform particle image velocimetry and traction stress microscopy to measure the velocity of cytoplasmic flow and the stresses applied to the substrate by migrating Physarum microamoebae. In parallel, we develop a mathematical model of a motile cell which includes forces from the viscous cytosol, a poro-elastic, contractile cytoskeleton and adhesive interactions with the substrate. Our experiments show that flow and traction stress exhibit back-to-front-directed waves with a distinct phase difference. The model demonstrates that the direction and speed of locomotion are determined by this coordination between contraction, flow and adhesion. Using the model, we identify forms of coordination that generate model predictions consistent with experiments. We demonstrate that this coordination produces near optimal migration speed and is insensitive to heterogeneity in substrate adhesiveness. While it is generally thought that amoeboid motility is robust to changes in extracellular geometry and the nature of extracellular adhesion, our results demonstrate that coordination of adhesive forces is essential to producing robust migration.

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Deakin, Nicholas O., and Christopher E. Turner. "Distinct roles for paxillin and Hic-5 in regulating breast cancer cell morphology, invasion, and metastasis." Molecular Biology of the Cell 22, no. 3 (February 2011): 327–41. http://dx.doi.org/10.1091/mbc.e10-09-0790.

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Individual metastatic tumor cells exhibit two interconvertible modes of cell motility during tissue invasion that are classified as either mesenchymal or amoeboid. The molecular mechanisms by which invasive breast cancer cells regulate this migratory plasticity have yet to be fully elucidated. Herein we show that the focal adhesion adaptor protein, paxillin, and the closely related Hic-5 have distinct and unique roles in the regulation of breast cancer cell lung metastasis by modulating cell morphology and cell invasion through three-dimensional extracellular matrices (3D ECMs). Cells depleted of paxillin by RNA interference displayed a highly elongated mesenchymal morphology, whereas Hic-5 knockdown induced an amoeboid phenotype with both cell populations exhibiting reduced plasticity, migration persistence, and velocity through 3D ECM environments. In evaluating associated signaling pathways, we determined that Rac1 activity was increased in cells devoid of paxillin whereas Hic-5 silencing resulted in elevated RhoA activity and associated Rho kinase–induced nonmuscle myosin II activity. Hic-5 was essential for adhesion formation in 3D ECMs, and analysis of adhesion dynamics and lifetime identified paxillin as a key regulator of 3D adhesion assembly, stabilization, and disassembly.

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Soll, David R., Deborah Wessels, Spencer Kuhl, and Daniel F. Lusche. "How a Cell Crawls and the Role of Cortical Myosin II." Eukaryotic Cell 8, no. 9 (July 24, 2009): 1381–96. http://dx.doi.org/10.1128/ec.00121-09.

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ABSTRACT The movements of Dictyostelium discoideum amoebae translocating on a glass surface in the absence of chemoattractant have been reconstructed at 5-second intervals and motion analyzed by employing 3D-DIAS software. A morphometric analysis of pseudopods, the main cell body, and the uropod provides a comprehensive description of the basic motile behavior of a cell in four dimensions (4D), resulting in a list of 18 characteristics. A similar analysis of the myosin II phosphorylation mutant 3XASP reveals a role for the cortical localization of myosin II in the suppression of lateral pseudopods, formation of the uropod, cytoplasmic distribution of cytoplasm in the main cell body, and efficient motility. The results of the morphometric analysis suggest that pseudopods, the main cell body, and the uropod represent three motility compartments that are coordinated for efficient translocation. It provides a contextual framework for interpreting the effects of mutations, inhibitors, and chemoattractants on the basic motile behavior of D. discoideum. The generality of the characteristics of the basic motile behavior of D. discoideum must now be tested by similar 4D analyses of the motility of amoeboid cells of higher eukaryotic cells, in particular human polymorphonuclear leukocytes.

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