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1 that are classified as either mesenchymal or amoeboid.
2 l for the migration of both mesenchymals and amoeboids.
3 enchymal cells create paths that are used by amoeboids.
4 -catalytic mechanism, MMP-9 promotes rounded-amoeboid 3D migration through regulation of actomyosin c
5 ithelial/mesenchymal (E/M), mesenchymal (M), amoeboid (A) and hybrid amoeboid/mesenchymal (A/M) pheno
6                           This was driven by amoeboid (activated) microglia, with no change in the de
7 e reduced, and microglia reverted from their amoeboid, active form to a ramified, resting configurati
8  while fs164 and fs120 cells adopted rounded/amoeboid and a mix of rounded and elongated morphologies
9 lin-1 (Nrp1) is expressed not on OPCs but on amoeboid and activated microglia in white but not gray m
10        Here we compare MMP levels in rounded-amoeboid and elongated-mesenchymal melanoma cells.
11 ions to maintain the precise balance between amoeboid and mesenchymal cell behaviors required for cel
12 found that melanoma cells can switch between amoeboid and mesenchymal forms via two different routes
13 ed in order to facilitate conversion between amoeboid and mesenchymal forms, as cells are either sear
14 TPases are required for the morphogenesis of amoeboid and mesenchymal forms, others are required for
15 g DOCK10 and Rac1 expression suppresses both amoeboid and mesenchymal migration and results in decrea
16 igated in the context of transitions between amoeboid and mesenchymal migration modes, which involve
17  elucidate novel roles of Cdc42 signaling in amoeboid and mesenchymal movement and tumor cell invasio
18 s can adopt two functionally distinct forms, amoeboid and mesenchymal, which facilitates their abilit
19 ferent phenotypes of motility and invasion - amoeboid and mesenchymal.
20 ctive pressures imposed by such organisms as amoeboid and nematode predators.
21                                         Both amoeboid and ramified cells from mesial temporal lobe ep
22                                              Amoeboid and spherical shapes represent perhaps the simp
23 lia are initially mitotic, rounded in shape (amoeboid), and phagocytically active.
24 F-beta, SMAD2 and its adaptor CITED1 control amoeboid behavior by regulating the expression of key ge
25 ransition and therefore suppresses efficient amoeboid bleb-based invasion.
26 ir ability to switch between mesenchymal and amoeboid (bleb-based) migration.
27 oflagellates subjected to confinement become amoeboid by retracting their flagella and activating myo
28 al cancer, hypoxia induces the transition to amoeboid cancer cell dissemination, yet the molecular me
29                                         Both amoeboid cancer cells and their associated macrophages s
30 alysis shows that ROCK-Myosin II activity in amoeboid cancer cells controls an immunomodulatory secre
31           It has been suggested that rounded-amoeboid cancer cells do not require matrix metalloprote
32 termediate filament network promotes LBBM of amoeboid cancer cells in confined environments and that
33 nhibition suppresses metastatic potential of amoeboid cancer cells in vivo, while a mitochondrial/AMP
34                             Mechanistically, amoeboid cancer cells perpetuate their behavior via ROCK
35                                      Rounded-amoeboid cancer cells use actomyosin contractility drive
36 l retina is characterized by the presence of amoeboid, carbonic anhydrase-positive microglial cells e
37 l cells undergo a series of conversions from amoeboid cell behaviors to more mesenchymal and finally
38 panin CD9 and facilitates the maintenance of amoeboid cell invasion.
39 as exhibited by fibroblasts is distinct from amoeboid cell migration and is characterized by dynamic
40 ially distinct microtubule dynamics regulate amoeboid cell migration by locally promoting the retract
41 ports a key role for lateral contractions in amoeboid cell motility, whereas the differences in their
42 ch to probe the basic molecular mechanism of amoeboid cell motility.
43 ay for evaluating the molecular mechanism of amoeboid cell motility.
44                                Rho-dependent amoeboid cell movement is a crucial mechanism in both tu
45 cal process involved in both cytokinesis and amoeboid cell movement.
46                 EMT-like and EMT-independent amoeboid cell subsets showed stable amoeboid movement ov
47 sarum polycephalum is a large multinucleated amoeboid cell that extends and develops pseudopods.
48                                              Amoeboid cell types are fundamental to animal biology an
49  MDA-MB-435S cells, with typical features of amoeboid cells (poor collagenolytic activity, rounded ce
50 Some responses perceived by 7TM receptors in amoeboid cells and possibly in human cells can initiate
51 s observed in regions of human tumours where amoeboid cells are disseminating.
52                                              Amoeboid cells are thought to find a path by deforming t
53 l directional decision-making in chemotactic amoeboid cells as a stimulus-dependent actin recruitment
54                         Leukocytes and other amoeboid cells change shape as they move, forming highly
55                                              Amoeboid cells change their cell shape during locomotion
56                                              Amoeboid cells have high levels of actomyosin contractil
57 hat, in the crawling of neutrophils or other amoeboid cells inside a micropipette, measurement of vel
58 possible modern analog is the aggregation of amoeboid cells into a migratory slug phase in cellular s
59 rs can lead to profound transformations from amoeboid cells into cells mimicking keratocytes, neurons
60                             Cell motility of amoeboid cells is mediated by localized F-actin polymeri
61 gical limitations, but finding such modes in amoeboid cells is more difficult as they lack these cons
62                      Following CSF1Ri, these amoeboid cells migrate radially and tangentially in a dy
63                                           As amoeboid cells migrate, signaling events such as Ras and
64 emonstrated that eukaryotic cells, including amoeboid cells of Dictyostelium discoideum and neutrophi
65     Microglial shape varied from ramified to amoeboid cells predominantly in regions of high neuronal
66                                              Amoeboid cells such as leukocytes can enter and migrate
67 rs, especially those of the integrin family, amoeboid cells such as leukocytes can migrate extremely
68                                 By contrast, amoeboid cells such as leukocytes use non-destructive st
69                  Migration of highly motile, amoeboid cells such as neutrophils has significant physi
70 of human and mouse melanomas are enriched in amoeboid cells that are also ki-67 positive.
71                      In nematodes, sperm are amoeboid cells that crawl via an extended pseudopod.
72 D. discoideum lives as haploid, free-living, amoeboid cells that divide asexually.
73 o motility system from Ascaris sperm, unique amoeboid cells that use filament arrays composed of majo
74 ltantly, the ubiquitous ability of mammalian amoeboid cells to migrate in two dimensions or three dim
75                           Therefore, rounded-amoeboid cells use both catalytic and non-catalytic acti
76 tensity and short-lived tractions exerted by amoeboid cells, such as dendritic cells.
77               Analogous to the chemotaxis of amoeboid cells, we found that a gradient of chemoattract
78 s of migration may be conserved in mammalian amoeboid cells.
79 yield signal amplification and adaptation in amoeboid cells.
80 ownstream effectors in metazoan, fungal, and amoeboid cells.
81 logous to that formed by actin in many other amoeboid cells.
82 ts analogous to that formed by actin in many amoeboid cells.
83 udopod formation and subsequent migration of amoeboid cells.
84 in: branched, putative Langerhans cells, and amoeboid cells.
85 singly, we found that pathways implicated in amoeboid chemotaxis, such as PI3K and mammalian target o
86   MMP-9 is upregulated in a panel of rounded-amoeboid compared with elongated-mesenchymal melanoma ce
87           Hypoxia induced calpain-2-mediated amoeboid conversion by deactivating B1 integrins through
88           Hypoxia induced calpain-2-mediated amoeboid conversion by deactivating beta1 integrins thro
89 -2 activity was required for hypoxia-induced amoeboid conversion in the orthotopic mouse dermis and u
90                              Hypoxia-induced amoeboid detachment was driven by hypoxia-inducible fact
91 for the pseudopod-dominated migration of the amoeboid Dictyostelium discoideum and for the lamellipod
92                              Hypoxia-induced amoeboid dissemination occurred through low extracellula
93 ypoxia-induced transition from collective to amoeboid dissemination of breast and head and neck (HN)
94 l cells migrating over a substratum crawl in amoeboid fashion; how the force against the substratum i
95  we find that in melanoma, TGF-beta promotes amoeboid features such as cell rounding, membrane blebbi
96 l cells increase migration speed by adopting amoeboid features.
97 onapoptotic membrane blebs, a feature of the amoeboid form of cell motility.
98 dynamics of the chemotactic migration of the amoeboid form of Dictyostelium discoideum.
99 to 1 microg ml(-1) LPS, most cells showed an amoeboid ('fried egg'-shaped) morphology with a 62% incr
100 lament system in regulating the migration of amoeboid human cancer cells.
101 enotype in treated animals, contrasting with amoeboid inflammatory and degenerative phenotype in untr
102 how that distinct from mesenchymal invasion, amoeboid invasion is independent of intracellular calpai
103 ells demonstrates that Net1A is required for amoeboid invasion, and loss of Net1A expression causes c
104 2-mediated integrin adhesion turnover during amoeboid invasion.
105 ion, and impair actomyosin contractility and amoeboid invasion.
106      Notably, melanoma can disseminate using amoeboid invasive strategies.
107 crest-stem cell transcriptional state and an amoeboid, invasive phenotype that increases seeding to t
108                                      Because amoeboid leader bleb-based migration (LBBM) occurs in co
109 hment of CSMD1 in the nerve growth cone, the amoeboid-leading edge of the growing neuron.
110         Different migration modes, including amoeboid-like and keratocyte-like, naturally emerge thro
111 ind that RhoC expression induces a primitive amoeboid-like cell invasion characterized by the formati
112 at the membrane-cortex traveling wave led to amoeboid-like cell migration.
113                 They also lack the customary amoeboid-like cell movements and active membrane project
114 /ROCK signalling, which specifically impairs amoeboid-like invasion, restores cell surface expression
115 than their parental counterparts and assumed amoeboid-like invasive abilities upon glycolysis inhibit
116                  Here we demonstrate that in amoeboid-like invasive tumour cell lines, the v-SNARE, V
117 ved in brain development, the here uncovered amoeboid-like migration mode might be conserved in other
118 on of LECs across a membrane (which involves amoeboid-like transmigration), it did not increase LEC c
119 cally reduces cell invasion, impairing both "amoeboid-like" and mesenchymal-like modes of invasion in
120 es are motile in two distinct modes: a fast "amoeboid-like" mode, which uses sequential discontinuous
121  migrate using different modes, ranging from amoeboid-like, during which actin filled protrusions com
122 dicating that Vannella represents a separate amoeboid lineage and the subclass Gymnamoebia is polyphy
123 lar processes, we show that many features of amoeboid locomotion emerge from a simple mechanochemical
124                                          The amoeboid locomotion of nematode sperm is mediated by the
125       In vitro, pre-PCs displayed processive amoeboid locomotion on surfaces coated with integrin lig
126 generate both of these central components of amoeboid locomotion.
127 crawling force generated by cells undergoing amoeboid locomotion.
128 nics in determining the emergent features of amoeboid locomotion.
129 s from a typical resting configuration to an amoeboid, macrophage-like morphology, increased expressi
130                    We propose eradication of amoeboid melanoma cells after surgical removal as a ther
131 ng genome-wide transcriptomics, we find that amoeboid melanoma cells are enriched in a TGF-beta-drive
132                         As a result, rounded-amoeboid melanoma cells degrade collagen I more efficien
133                                 Importantly, amoeboid melanoma cells express both proliferative and i
134           Surprisingly, we find that rounded-amoeboid melanoma cells secrete higher levels of several
135 ulator Cdc42EP5 is consistently required for amoeboid melanoma cells to invade and migrate into colla
136 sis of human melanoma biopsies revealed that amoeboid melanoma cells with high Myosin II activity are
137 ing abilities are characteristic of invasive amoeboid melanoma cells.
138 e the circuit's three possible states to the amoeboid, mesenchymal and amoeboid/mesenchymal hybrid ph
139 M), mesenchymal (M), amoeboid (A) and hybrid amoeboid/mesenchymal (A/M) phenotypes.
140 ible states to the amoeboid, mesenchymal and amoeboid/mesenchymal hybrid phenotype.
141 on in MTLn3 cells (an apolar randomly moving amoeboid metastatic tumor cell) caused them to extend pr
142 t, there is an increase in ferritin-positive amoeboid microglia and a decrease in immunohistochemical
143                                              Amoeboid microglia and disrupted astrocyte meshwork are
144                         In summary, reactive/amoeboid microglia are the most represented population i
145 d differentiation, is expressed in forebrain amoeboid microglia during the first two postnatal weeks.
146 nd white matter areas of the brain, but only amoeboid microglia in discrete foci in the subcortical w
147 ssociated with accumulation of ERK-activated amoeboid microglia in mice, and is also observed in huma
148 omyelinase knockout (ASMko) mouse model show amoeboid microglia in neurodegeneration-prone areas.
149  and an increase in the ratio of ramified to amoeboid microglia in the thalamus.
150                         Runx1 inhibits mouse amoeboid microglia proliferation and promotes progressio
151                 At the cellular level, fewer amoeboid microglia/macrophages appeared adjacent to the
152 t is densely populated with intermediate and amoeboid microglia; the latter is indicative of an activ
153 le is known about the mechanisms controlling amoeboid microglial cell proliferation, activation, and
154 , collective, and single-cell mesenchymal or amoeboid migration [2-4].
155 ccur in many physiological contexts, such as amoeboid migration and cytokinesis.
156 chyme transition that involves activation of amoeboid migration and loss of cell-cell adhesion.
157 tatin-induced vimentin bundling inhibit fast amoeboid migration and proliferation.
158             However, the role of vimentin in amoeboid migration has not been determined.
159           ROCK-Myosin II drives fast rounded-amoeboid migration in cancer cells during metastatic dis
160 dhering to it, and which may be relevant for amoeboid migration in complex three-dimensional environm
161                                         Fast amoeboid migration is critical for developmental process
162 asma membrane, the percentage of cells using amoeboid migration is further increased in undulating mi
163                                          How amoeboid migration is regulated by extracellular signals
164 nsional migration and the 3-dimensional (3D) amoeboid migration mode of HIV-1-infected human monocyte
165 last spreading through either mesenchymal or amoeboid migration modes.
166 ykinin during glioma invasion by stimulating amoeboid migration of glioma cells.
167 cortex contractility plays a crucial role in amoeboid migration of metastatic cells [6] and during di
168 mal cells can spontaneously switch to a fast amoeboid migration phenotype.
169                                         Fast amoeboid migration requires cells to apply mechanical fo
170    Immune cell locomotion is associated with amoeboid migration, a flexible mode of movement, which d
171 en thoroughly investigated in the context of amoeboid migration, but it has been examined far less in
172 f reduced integrin-dependent migration, i.e. amoeboid migration, is a known phenotype.
173 le organizing centre is a typical feature of amoeboid migration, our findings link the fundamental or
174 anges, but in contrast to other instances of amoeboid migration, trailing edge retraction involves ep
175 s distinct from conventional mesenchymal and amoeboid migration, whereby long-lived episodes of slow,
176 exible vimentin network is required for fast amoeboid migration.
177 ve and quantify wave-like characteristics of amoeboid migration.
178 or mesenchymal migration but dispensable for amoeboid migration.
179  SCAR/WAVE complex plays in the mechanics of amoeboid migration.
180 ng to increased actomyosin contractility and amoeboid migration.
181 s actin remodeling factors required for fast amoeboid migration.
182  Phosphatase, increasing Myosin II-dependent amoeboid migration.
183 ch, dendritic cells perform a random walk by amoeboid migration.
184 fied DOCK10, a Cdc42 GEF, as a key player in amoeboid migration; accordingly, we find that expression
185 tic dissemination of cancer cells, and fast "amoeboid" migration in the invasive fronts of tumors is
186 y use the protease- and podosome-independent amoeboid mode in more porous matrices.
187  promoted the transition from mesenchymal to amoeboid mode of movement as well as augmented phagocyto
188 s and actin fiber traction, whereas the fast amoeboid mode, observed exclusively for leukocytes and c
189 cantly higher capacity to transition into an amoeboid mode.
190 D) environment in either mesenchymal-type or amoeboid modes.
191            This occurs through a mesenchymal-amoeboid morphological switch that signals through the R
192  surveillant microglia undergo a ramified-to-amoeboid morphological transformation and become phagocy
193 omoted microglial activation, as assessed by amoeboid morphology and increased expression of MHC clas
194                                              Amoeboid morphology and the consequent loss of microglia
195 cells, with colonial cells exhibiting a more amoeboid morphology consistent with higher levels of mac
196 ted microglia to assume their characteristic amoeboid morphology during brain inflammation.
197 on leads to increased microglial numbers and amoeboid morphology in the DG.
198                                Such PAM have amoeboid morphology, are metabolically active, and phago
199 ed by WNV infection, as exemplified by their amoeboid morphology, the development of filopodia and la
200 assays, with cells expressing TNCEGFL having amoeboid morphology.
201 CCL2hi tg+ mice were defective in expressing amoeboid morphology.
202 ntexts, protrusions adopt lamellipodia or an amoeboid morphology.
203 g complexes associated with phagocytosis and amoeboid motility and also reveals a conspicuous expansi
204 est the hypothesis that AQP-1 is involved in amoeboid motility and angiogenic invasion during cirrhos
205 nto the machinery needed for pseudopod-based amoeboid motility and how it evolved.
206 sperm protein (MSP) of Ascaris suum mediates amoeboid motility by forming an extensive intermeshed sy
207 sperm protein (MSP) of Ascaris suum mediates amoeboid motility by forming an extensive intermeshed sy
208 K activation during planar cell movement and amoeboid motility during extracellular matrix (ECM) inva
209                              Cells employing amoeboid motility exhibit repetitive cycles of rapid exp
210 n bone marrow (BM) was strictly dependent on amoeboid motility mediated by CXCR4 and CXCL12 and by al
211          The major sperm protein (MSP)-based amoeboid motility of Ascaris suum sperm requires coordin
212 in, a cytoskeletal molecule required for the amoeboid motility of sperm in Caenorhabditis elegans, al
213  Here, we report that septins participate in amoeboid motility of T cells, enabling the formation of
214              However, the exact mechanism of amoeboid motility remains elusive.
215                                              Amoeboid motility requires spatiotemporal coordination o
216             Myosin-IIA is necessary for fast amoeboid motility, and our data suggests that this occur
217                                          For amoeboid motility, lymphocytes do not require specific b
218 cytoskeletal element's role during effective amoeboid motility.
219 ependently in eukaryotes that evolved active amoeboid motility.
220 f Arp2/3-nucleated actin networks that drive amoeboid motility.
221 ver, we construct a comprehensive catalog of amoeboid-motility genes.
222 ge microscopic technique and showed they had amoeboid movement and phagocytic abilities.
223 s that control the activation of GTPases for amoeboid movement are poorly understood, we sought to id
224 sociated neurons use somal translocation and amoeboid movement as they migrate to their final positio
225 erstood, we sought to identify regulators of amoeboid movement by screening an siRNA library targetin
226                                              Amoeboid movement is characterized by relatively non-pol
227              Induced by metabolic challenge, amoeboid movement may thus constitute a common endpoint
228                                   How is the amoeboid movement of lymphocytes in secondary lymphoid o
229 ependent amoeboid cell subsets showed stable amoeboid movement over hours as well as leukocyte-like t
230  to direct mesenchymal movement and suppress amoeboid movement through decreasing actomyosin contract
231               Transition from mesenchymal to amoeboid movement was associated with decreased levels o
232                                           In amoeboid movement, cells have a rounded morphology, are
233                               Conversely, in amoeboid movement, Rho-kinase signaling activates a Rac
234 rix (ECM)-adhesive, predominantly bleb-based amoeboid movement, which was maintained by a low-oxidati
235  of protoplasm of conical form, endowed with amoeboid movements.
236 sition (CAT), promoting the dissemination of amoeboid-moving single cells from collective invasion st
237 also increased in csf1r-mutants, exclusively amoeboid mpeg1+ cells were present, which we showed by g
238             In the postnatal brain, immature amoeboid myeloid precursors only induce SPARC expression
239               These results suggest that the amoeboid myosin I consensus phosphorylation site and SH3
240 ension, and those that mildly overexpress an amoeboid myosin I exhibit increased cortical tension.
241                                          The amoeboid myosin I's are required for cellular cortical f
242                               Given that the amoeboid myosin I's possess both actin- and membrane-bin
243 elium cells either lacking or overexpressing amoeboid myosin Is have significant defects in cortical
244                                              Amoeboid myosin Is play a critical role in regulating ps
245                                              Amoeboid Olivine Aggregates (AOAs) have never been melte
246 m-rich inclusion (CAI) accretionary rims and amoeboid olivine aggregates (AOAs), are oxygen-16 (16O)
247 itions via the apolar or polar route and not amoeboid or mesenchymal morphogenesis per se.
248 extracellular proteases; however, cells with amoeboid or rounded morphologies are able to invade even
249 n correlated with a reduced number of Cox-2+ amoeboid phagocytes adjacent to the injury.
250 icroglia reduced microglial activation to an amoeboid phenotype and decreased the phagocytosis of inj
251 eformable environments, tumor cells adopt an amoeboid phenotype and release microvesicles.
252  CITED1 is coupled to a contractile-rounded, amoeboid phenotype in a panel of 16 melanoma cell lines,
253 n elongated/mesenchymal phenotype to a round/amoeboid phenotype in the absence of similar effects on
254 ocytoma cells resulted in a transition to an amoeboid phenotype that was abolished with the ROCK inhi
255 olon cancer cells are able to transfer their amoeboid phenotype to isogenic primary cancer cells thro
256 rphology, whereas Hic-5 knockdown induced an amoeboid phenotype with both cell populations exhibiting
257       Cancer cells with rapid PNI exhibit an amoeboid phenotype, highlighting the plasticity of cance
258 RASAL2 knockdown leads to a conversion to an amoeboid phenotype.
259  required for the maintenance of the rounded-amoeboid phenotype.
260  population of mesenchymals kept in a mostly-amoeboid population.
261 d of host-microbe interactions that includes amoeboid predation and endosymbiotic existence.
262 acquired microbes, biotic pressures, such as amoeboid predators, may select for the capacity for viru
263 ating the RhoA/ROCK pathway, known to induce amoeboid properties and destabilization of endothelial j
264 algae, a green alga and a relatively derived amoeboid protist.
265 icroscopy showed that Ptpro(-/-) mice had an amoeboid rather than the typical octopoid structure seen
266 he defined target, for different mesenchymal/amoeboid ratios.
267 ctive intervention to combat hypoxia-induced amoeboid reprogramming remain unclear.
268       We show that the incredible variety in amoeboid shape across a population can be reduced to a f
269                       Endoderm cells move by amoeboid shape changes, but in contrast to other instanc
270  preservation of brain volume, a decrease in amoeboid-shaped microglia in the dentate gyrus and an in
271                                              Amoeboid sperm crawl around fertilized eggs to the sperm
272               Leading edge protrusion in the amoeboid sperm of Ascaris suum is driven by the localize
273 pment and motility of Caenorhabditis elegans amoeboid sperm.
274  unpolarized round spermatids into polarized amoeboid spermatozoa capable of both motility and fertil
275 he developmental cycle and when cells in the amoeboid stage are subjected to stress but the phosphory
276 rity and B1 integrin engagement and reverted amoeboid to elongated phenotypes under hypoxia.
277 y and beta1 integrin engagement and reverted amoeboid to elongated phenotypes under hypoxia.
278 ts, thereby reducing the period required for amoeboid-to-mesenchymal transition.
279 mors [9], as an inducer of the collective-to-amoeboid transition (CAT), promoting the dissemination o
280 n phenotypes, specifically the Collective-to-Amoeboid Transition (CAT).
281 enchymal Transition (EMT) and Mesenchymal-to-Amoeboid Transition (MAT) - have been carefully investig
282                              The mesenchymal-amoeboid transition (MAT) was proposed as a mechanism fo
283 ion of activated Cdc42 induces a mesenchymal-amoeboid transition and increases cell invasion.
284 tomyosin levels and favours an epithelial to amoeboid transition contributing to tumour aggressivenes
285 7E in melanoma cells led to a mesenchymal-to-amoeboid transition driven by Cdc42 activation.
286                However, direct epithelial to amoeboid transition has not been characterized to date.
287 al that ECT2 has a novel role in mesenchymal-amoeboid transition in human astrocytoma cells.
288 hly metastatic cancer, undergo epithelial to amoeboid transition in physiological environments, such
289              The induction of mesenchymal-to-amoeboid transition promoted melanoma cell invasion, sur
290 tance to be associated with a mesenchymal-to-amoeboid transition switch, upregulation of Cdc42 activi
291 tates vs the capacity of confined migration, amoeboid transition, and cellular stiffness.
292 ting into confinement undergo mesenchymal-to-amoeboid transition.
293  some tumour cells undergo a 'mesenchymal to amoeboid' transition that allows invasion in the absence
294 ontexts including mitosis and mesenchymal-to-amoeboid transitions.
295         Hence, the loss of cofilin caused an amoeboid tumor cell to assume a mesenchymal-type mode of
296                         Herein, we show that amoeboid tumor cells export large (1- to 10-mum diameter
297                                              Amoeboid tumor cells generate sufficient actomyosin forc
298                 Emerging research implicates amoeboid-type motility and membrane blebbing as features
299  termination of the planktonic life cycle in amoeboid, unarthropodal stages, evolved convergently and
300 g apparent that some cancer cells move in an amoeboid way similar to leukocytes.

 
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