Increase In Migration Speed Research Articles

RapB Regulates Cell Adhesion and Migration in Dictyostelium, Similar to RapA.

Ras small GTPases act as molecular switches in various cellular signaling pathways, including cell migration, proliferation, and differentiation. Three Rap proteins are present in Dictyostelium; RapA, RapB, and RapC. RapA and RapC have been reported to have opposing functions in the control of cell adhesion and migration. Here, we investigated the role of RapB, a member of the Ras GTPase subfamily in Dictyostelium, focusing on its involvement in cell adhesion, migration, and developmental processes. This study revealed that RapB, similar to RapA, played a crucial role in regulating cell morphology, adhesion, and migration. rapB null cells, which were generated by CRISPR/Cas9 gene editing, displayed altered cell size, reduced cell-substrate adhesion, and increased migration speed during chemotaxis. These phenotypes of rapB null cells were restored by the expression of RapB and RapA, but not RapC. Consistent with these results, RapB, similar to RapA, failed to rescue the phenotypes of rapC null cells, spread morphology, increased cell adhesion, and decreased migration speed during chemotaxis. Multicellular development of rapB null cells remained unaffected. These results suggest that RapB is involved in controlling cell morphology and cell adhesion. Importantly, RapB appears to play an inhibitory role in regulating the migration speed during chemotaxis, possibly by controlling cell-substrate adhesion, resembling the functions of RapA. These findings contribute to the understanding of the functional relationships among Ras subfamily proteins.

Paracrine Ovarian Cancer Cell-Derived CSF1 Signaling Regulates Macrophage Migration Dynamics in a 3D Microfluidic Model that Recapitulates In Vivo Infiltration Patterns in Patient-Derived Xenografts.

A high density of macrophages in the ovarian cancer microenvironment is associated with disease progression and poor outcomes. Understanding cancer-macrophage interaction mechanisms that establish this pro-tumorigenic microenvironment is critical for developing macrophage-targeted therapies. Here, 3D microfluidic assays and patient-derived xenografts are utilized to define the role of cancer-derived colony stimulating factor 1 (CSF1) on macrophage infiltration dynamics toward ovarian cancer cells. It is demonstrated that multiple ovarian cancer models promote the infiltration of macrophages into a 3D extracellular matrix in vitro in a cell density-dependent manner. Macrophages exhibit directional migration and increased migration speed under both direct interactions with cancer cells embedded within the matrix and paracrine crosstalk with cancer cells seeded in an independent microchannel. It is also found that platinum-based chemotherapy increases macrophage recruitment and the levels of cancer cell-derived CSF1. Targeting CSF1 signaling under baseline or chemotherapy-treatment conditions reduces the number of infiltrated macrophages. It is further shown that results obtained with the 3D microfluidic model reflect the recruitment profiles of macrophages in patient-derived xenografts in vivo. These findings highlight the role of CSF1 signaling in establishing macrophage-rich ovarian cancer microenvironments, as well as the utility of microfluidic models in recapitulating 3D tumor ecosystems and dissecting cancer-macrophage signaling.

Dynamics of endothelial cells migration in nature-mimicking blood vessels

Endothelial cells (ECs) migration is a crucial early step in vascular repair and tissue neovascularization. While extensive research has elucidated the biochemical drivers of endothelial motility, the impact of biophysical cues, including vessel geometry and topography, remains unclear. Herein, we present a novel approach to reconstruct 3D self-assembly blood vessels-on-a-chip that accurately replicates real vessel geometry and topography, surpassing conventional 2D flat tube formation models. This vessels-on-a-chip system enables real-time monitoring of vasculogenesis and ECs migration at high spatiotemporal resolution. Our findings reveal that ECs exhibit increased migration speed and directionality in response to narrower vessel geometries, transitioning from a rounded to a polarized morphology. These observations underscore the critical influence of vessel size in regulating ECs migration and morphology. Overall, our study highlights the importance of biophysical factors in shaping ECs behavior, emphasizing the need to consider such factors in future studies of endothelial function and vessel biology.

SPAK-dependent cotransporter activity mediates capillary adhesion and pressure during glioblastoma migration in confined spaces.

The invasive potential of glioblastoma cells is attributed to large changes in pressure and volume, driven by diverse elements, including the cytoskeleton and ion cotransporters. However, how the cell actuates changes in pressure and volume in confinement, and how these changes contribute to invasive motion is unclear. Here, we inhibited SPAK activity, with known impacts on the cytoskeleton and cotransporter activity and explored its role on the migration of glioblastoma cells in confining microchannels to model invasive spread through brain tissue. First, we found that confinement altered cell shape, inducing a transition in morphology that resembled droplet interactions with a capillary vessel, from "wetting" (more adherent) at low confinement, to "nonwetting" (less adherent) at high confinement. This transition was marked by a change from negative to positive pressure by the cells to the confining walls, and an increase in migration speed. Second, we found that the SPAK pathway impacted the migration speed in different ways dependent upon the extent of wetting. For nonwetting cells, SPAK inhibition increased cell-surface tension and cotransporter activity. By contrast, for wetting cells, it also reduced myosin II and YAP phosphorylation. In both cases, membrane-to-cortex attachment is dramatically reduced. Thus, our results suggest that SPAK inhibition differentially coordinates cotransporter and cytoskeleton-induced forces, to impact glioblastoma migration depending on the extent of confinement.

Sensory nerves enhance triple-negative breast cancer invasion and metastasis via the axon guidance molecule PlexinB3

In breast cancer, nerve presence has been correlated with more invasive disease and worse prognosis, yet the mechanisms by which different types of peripheral nerves drive tumor progression remain poorly understood. In this study, we identified sensory nerves as more abundant in human triple-negative breast cancer (TNBC) tumors. Co-injection of sensory neurons isolated from the dorsal root ganglia (DRG) of adult female mice with human TNBC cells in immunocompromised mice increased the number of lung metastases. Direct in vitro co-culture of human TNBC cells with the dorsal root ganglia (DRG) of adult female mice revealed that TNBC cells adhere to sensory neuron fibers leading to an increase in migration speed. Species-specific RNA sequencing revealed that co-culture of TNBC cells with sensory nerves upregulates the expression of genes associated with cell migration and adhesion in cancer cells. We demonstrated that lack of the semaphorin receptor PlexinB3 in cancer cells attenuate their adhesion to and migration on sensory nerves. Together, our results identify a mechanism by which nerves contribute to breast cancer migration and metastasis by inducing a shift in TNBC cell gene expression and support the rationale for disrupting neuron-cancer cell interactions to target metastasis.

Breeding and migration performance metrics highlight challenges for White-naped Cranes

Globally, habitat loss has been deemed a major threat to wetland bird populations. However, the underlying mechanism of population declines and variations in the birds’ vulnerability throughout their annual cycle is challenging to determine, yet critical for development of targeted conservation strategies. Over seven years, landscape water availability explained occupancy of breeding territories best when breeding performance, migratory performance, and annual survival of the White-naped Crane (Grus vipio) population in eastern Mongolia were studied. Also, the hatching success of eggs was positively correlated with water availability in addition to plant productivity. High ambient temperatures and large numbers of herder families (and hence more livestock) negatively affected hatching success. High water availability at Luan, a major stopover site increased migration speed during the cranes’ northbound migration to their breeding grounds. In contrast, when water conditions were favorable, the birds stayed longer at the stopover site during southbound migration. Increased human density reduced the use of the stopover site during northbound migration. Finally, cranes arrived early at the breeding grounds when ambient temperature was high in northeast Mongolia. Combining these findings with historical trends in key environmental factors on their breeding grounds explains the general decline observed in this population of cranes in recent decades. Extrapolating our findings with future climate predictions, the outlook seems poor unless urgent action is taken. Knowledge of the mechanisms underlying White-naped Crane population decline in eastern Mongolia identified in this paper should improve the effectiveness of these actions.

Effects of different protocols of defocused high-power laser on the viability and migration of myoblasts-a comparative in vitro study.

The aim of the present study was to analyze for the first time the effect of photobiomodulation therapy (PBMT) using defocused high-power laser (DHPL) in myoblast cell line C2C12 viability and migration and compare them with low-power laser therapy. Cells were divided into 9 groups: Sham irradiation 10% fetal bovine serum (FBS); Sham irradiation 5%FBS; low-power laser 0.1W; DHPL 810 1W; DHPL 810 2W; DHPL 980 1W; DHPL 980 2W; DHPL dual 1W; DHPL dual 2W. To simulate stress conditions, all groups exposed to irradiation were maintained in DMEM 5% FBS. The impact of therapies on cell viability was assessed through sulforhodamine B assay and on cells migration through scratch assays and time-lapse. Myoblast viability was not modified by PBMT protocols. All PBMT protocols were able to accelerate the scratch closure after 6 and 18h of the first irradiation (p < 0.001). Also, an increase in migration speed, with a more pronounced effect of DHPL laser using dual-wavelength protocol with 2W was observed (p < 0.001). In conclusion, the diverse PBMT protocols used in this study accelerated the C2C12 myoblasts migration, with 2-W dual-wavelength outstanding as the most effective protocol tested. Benefits from treating muscle injuries with PBMT appear to be related to its capacity to induce cell migration without notable impact on cell viability.

EFFECTS OF LOW-POWER AND DEFOCUSED HIGH-POWER LASER ON THE VIABILITY AND MIGRATION OF MYOBLASTS—A COMPARATIVE IN VITRO STUDY

<h3>Objectives</h3> The aim of the present study was to analyze the effect of different photobiomodulation (PBM) therapies in myoblast cell line C2C12 viability and migration. <h3>Study Design</h3> Cells were divided into 9 groups: sham irradiation 10% fetal bovine serum (FBS); sham irradiation 5% FBS; low-level laser 0.1 W; defocused high-power laser (DHPL) 810 1 W; 810 2 W; 980 1 W; 980 2 W; dual 1 W; dual 2 W. To simulate stress conditions, all groups exposed to irradiation were maintained in Dulbecco's Modified Eagle Medium (DMEM) 5% FBS. The impact of therapies on cell viability was assessed through sulforhodamine B assay and on cell migration through scratch assays and time lapse. <h3>Results</h3> Myoblast viability was not modified by PBM protocols. All PBM protocols were able to accelerate wound closure 6 and 18 hours after the first irradiation (<i>P</i> < .001). Also, an increase in migration speed, with a more pronounced effect of DHPL using dual wavelength protocol with 1 W, was observed (<i>P</i> < .001). <h3>Conclusions</h3> Diverse PBM protocols accelerated C2C12 myoblast migration, with GD1W outstanding as the most effective protocol tested. Benefits from treating muscle injuries with PBM appear to be related to its capacity to induce cell migration without a notable impact on cell viability.

The Effects of Viscoelasticity on Droplet Migration on Surfaces with Wettability Gradients.

A finite-volume method based on the OpenFOAM is used to numerically study the factors affecting the migration of viscoelastic droplets on rigid surfaces with wettability gradients. Parameters investigated include droplet size, relaxation time, solvent viscosity, and polymer viscosity of the liquid comprising droplets. The wettability gradient is imposed numerically by assuming a linear change in the contact angle along the substrate. As reported previously for Newtonian droplets, the wettability gradient induces spontaneous migration from hydrophobic to hydrophilic region on the substrate. The migration of viscoelastic droplets reveals the increase in the migration speed and distance with the increase in the Weissenberg number. The increase in droplet size also shows the increase in both the migration speed and distance. The increase in polymer viscosity exhibits the increase in migration speed but the decrease in migration distance.

The amoeboid state as part of the epithelial-to-mesenchymal transition programme.

Cell migration is essential for many biological processes, while abnormal cell migration is characteristic of cancer cells. Epithelial cells become motile by undergoing epithelial-to-mesenchymal transition (EMT), and mesenchymal cells increase migration speed by adopting amoeboid features. This review highlights how amoeboid behaviour is not merely a migration mode but rather a cellular state - within the EMT spectra - by which cancer cells survive, invade and colonise challenging microenvironments. Molecular biomarkers and physicochemical triggers associated with amoeboid behaviour are discussed, including an amoeboid associated tumour microenvironment. We reflect on how amoeboid characteristics support metastasis and how their liabilities could turn into therapeutic opportunities.

Metastasising Fibroblasts Show an HDAC6-Dependent Increase in Migration Speed and Loss of Directionality Linked to Major Changes in the Vimentin Interactome

Metastasising cells express the intermediate filament protein vimentin, which is used to diagnose invasive tumours in the clinic. We aimed to clarify how vimentin regulates the motility of metastasising fibroblasts. STED super-resolution microscopy, live-cell imaging and quantitative proteomics revealed that oncogene-expressing and metastasising fibroblasts show a less-elongated cell shape, reduced cell spreading, increased cell migration speed, reduced directionality, and stronger coupling between these migration parameters compared to normal control cells. In total, we identified and compared 555 proteins in the vimentin interactome. In metastasising cells, the levels of keratin 18 and Rab5C were increased, while those of actin and collagen were decreased. Inhibition of HDAC6 reversed the shape, spreading and migration phenotypes of metastasising cells back to normal. Inhibition of HDAC6 also decreased the levels of talin 1, tropomyosin, Rab GDI β, collagen and emilin 1 in the vimentin interactome, and partially reversed the nanoscale vimentin organisation in oncogene-expressing cells. These findings describe the changes in the vimentin interactome and nanoscale distribution that accompany the defective cell shape, spreading and migration of metastasising cells. These results support the hypothesis that oncogenes can act through HDAC6 to regulate the vimentin binding of the cytoskeletal and cell–extracellular matrix adhesion components that contribute to the defective motility of metastasising cells.

МНОГООБРАЗИЕ ГЕНДЕРНЫХ РОЛЕЙ В СОВРЕМЕННОМ МИРЕ И ИХ ОТРАЖЕНИЕ В НЕМЕЦКОМ ЯЗЫКЕ

The increased migration speed, occupational labor mobility, the declining importance of family and religious affiliation, the migration policy and the global political situation are accelerating social disorders in Germany. Globalisation, computerisation and digitalisation have brought cultural interaction and communication to a new level and launched various new mechanisms for the progress of both society and language. Fundamental social changes are being reflected in language. These shifts are accompanied by the evolution of language and on governmental “Language Policy”, conceptually by megatrends, interpreted as complex social transformation processes. These changes, based on concepts such as “Political Correctness”, “Light and Plain German”, gender-neutral wording and gender equality are reflected in the German language.

The WASp L272P gain-of-function mutation alters dendritic cell coordination of actin dynamics for migration and adhesion.

Dendritic cells (DCs) devoid of the actin regulator Wiskott-Aldrich syndrome protein (WASp) show reduced directed migration and decreased formation of podosome adhesion structures. We examined DCs expressing a gain-of-function mutation in WASp, WASp L272P, identified in X-linked neutropenia patients. Analysis of WASp L272P DCs was compared to WASp-deficient DCs to examine how WASp activity influences DC migratory responses. In confined space, WASp-deficient DCs had increased migration speed whereas WASp L272P DCs had similar average speed but increased speed fluctuations, reduced displacement, and atypical rounded morphology, compared to wild-type (WT) DCs. Using an ear inflammation model and flow cytometry analysis, WT, WASp-deficient, and WASp L272P DCs were found to migrate in comparable numbers to the draining lymph nodes (LNs). However, histology analysis revealed that migratory DCs of WASp deficient and WASp L272P mice were mainly located in the collagenous capsule of the LN whereas WT DCs were located inside the LN. Analysis of ultrastructural features revealed that WASp L272P DCs had reduced cell area but formed larger podosome structures when compared to WT DCs. Together, our data suggest that WASp activity regulates DC migration and that loss-of-function and gain-of-function in WASp activity lead to different and phenotype-specific DC migratory behavior.

Widespread shifts in bird migration phenology are decoupled from parallel shifts in morphology.

Advancements in phenology and changes in morphology, including body size reductions, are among the most commonly described responses to globally warming temperatures. Although these dynamics are routinely explored independently, the relationships among them and how their interactions facilitate or constrain adaptation to climate change are poorly understood. In migratory species, advancing phenology may impose selection on morphological traits to increase migration speed. Advancing spring phenology might also expose species to cooler temperatures during the breeding season, potentially mitigating the effect of a warming global environment on body size. We use a dataset of birds that died after colliding with buildings in Chicago, IL to test whether changes in migration phenology are related to documented declines in body size and increases in wing length in 52 North American migratory bird species between 1978 and 2016. For each species, we estimate temporal trends in morphology and changes in the timing of migration. We then test for associations between species-specific rates of phenological and morphological changes while assessing the potential effects of migratory distance and breeding latitude. We show that spring migration through Chicago has advanced while the timing of fall migration has broadened as a result of early fall migrants advancing their migrations and late migrants delaying their migrations. Within species, we found that longer wing length was linked to earlier spring migration within years. However, we found no evidence that rates of phenological change across years, or migratory distance and breeding latitude, are predictive of rates of concurrent changes in morphological traits. These findings suggest that biotic responses to climate change are highly multidimensional and the extent to which those responses interact and influence adaptation to climate change requires careful examination.

Unexpected localization of AQP3 and AQP4 induced by migration of primary cultured IMCD cells

Aquaporin-2–4 (AQP) are expressed in the principal cells of the renal collecting duct (CD). Beside their role in water transport across membranes, several studies showed that AQPs can influence the migration of cells. It is unknown whether this also applies for renal CD cells. Another fact is that the expression of these AQPs is highly modulated by the external osmolality. Here we analyzed the localization of AQP2–4 in primary cultured renal inner medullary CD (IMCD) cells and how osmolality influences the migration behavior of these cells. The primary IMCD cells showed a collective migration behavior and there were no differences in the migration speed between cells cultivated either at 300 or 600 mosmol/kg. Acute increase from 300 to 600 mosmol/kg led to a marked reduction and vice versa an acute decrease from 600 to 300 mosmol/kg to a marked increase in migration speed. Interestingly, none of the analyzed AQPs were localized at the leading edge. While AQP3 disappeared within the first 2–3 rows of cells, AQP4 was enriched at the rear end. Further analysis indicated that migration induced lysosomal degradation of AQP3. This could be prevented by activation of the protein kinase A, inducing localization of AQP3 and AQP2 at the leading edge and increasing the migration speed.

FilGAP, a GAP protein for Rac, regulates front-rear polarity and tumor cell migration through the ECM.

Migrating tumor cells are characterized by a sustained front-rear asymmetry, with a front enriched in filamentous actin, which is induced by Rho small GTPase Rac. Regulation of Rac activity by its regulators should be required for effective motility. Here, we show that FilGAP, a GTPase-activating protein (GAP) for Rac, controls front-rear polarity and contributes to maintain effective tumor cell migration through the extracellular matrix (ECM). Overexpression of FilGAP in breast cancer cells induced polarized morphology and led to increased migration speed in collagen matrices, while depletion of FilGAP impaired the cell polarity and migration. FilGAP localizes to the cell front through its pleckstrin-homology (PH) domain in a phosphatidylinositol 3,4,5-trisphosphate (PIP3)-dependent manner and appears to inactivate Rac at its site. We found that the affinity of PH domain to PIP3 is critically involved in the maintenance of cell polarity. Moreover, small GTPase ADP-ribosylation factor 6 (Arf6), which binds to the FilGAP PH domain, also regulates FilGAP-mediated cell polarity and migration of breast cancer cells. We propose that FilGAP regulates front-rear polarity through its PIP3 and Arf6 binding in tumor cell migration through the ECM.

Increased Corneal Endothelial Cell Migration in Fuchs Endothelial Corneal Dystrophy: A Live Cell Imaging Study

PurposeTo investigate if corneal endothelial cells (CECs) in Fuchs endothelial corneal dystrophy (FECD) have altered cellular migration compared with normal controls.DesignComparative analysis.MaterialsDescemet’s membrane and CECs derived from patients with FECD undergoing endothelial keratoplasty or normal cadaveric donors.MethodsEx vivo specimens were used for live cell imaging and generation of immortalized cell lines. Live imaging was performed on FECD and normal CECs and on ex vivo specimens transfected with green fluorescent protein. Migration speeds were determined as a function of cellular density using automated cell tracking. Ex vivo specimens were classified as either FECD or normal low cell density (nonconfluent) or high cell density (confluent). Scratch assay was performed on CECs seeded at high confluence to determine migration speed. Genetic analysis from blood samples or CECs was performed to detect a CTG repeat expansion in the TCF4 gene.Main Outcome MeasuresMean cell migration speed.ResultsFuchs endothelial corneal dystrophy CECs in low cell density areas displayed increased mean speed (0.391 ± 0.005 μm/minute vs. 0.364 ± 0.005 μm/minute; P < 0.001) and mean maximum speed (0.961 ± 0.010 μm/minute vs. 0.787 ± 0.011 μm/minute; P < 0.001) compared with normal CECs, and increased mean maximum speed (0.778 ± 0.014 μm/minute vs. 0.680 ± 0.011 μm/minute; P < 0.001) in high cell density areas ex vivo. Similarly, FECD CECs displayed increased mean speed compared with normal CECs (1.958 ± 0.020 μm/minute vs. 2.227 ± 0.021 μm/minute vs. 1.567 ± 0.019 μm/minute; P < 0.001) under nonconfluent conditions in vitro. Moreover, FECD CECs also displayed increased mean speed compared with normal CECs under high confluent conditions as detected by scratch assay (37.2 ± 1.1% vs. 44.3 ± 4.1% vs. 70.7 ± 5.2%; P < 0.001). Morphologic analysis showed that FECD CECs displayed an increased fibroblastic phenotype as detected by filamentous-actin labeling.ConclusionsFuchs endothelial corneal dystrophy CECs demonstrated increased migration speed compared with normal CECs. Further investigation into the mechanisms of heightened cell migration in FECD is needed and may provide insight into its pathogenesis, as well as having implications on descemetorhexis without endothelial keratoplasty.

Arhgef6 (alpha-PIX) cytoskeletal regulator signals to GTPases and Cofilin to couple T cell migration speed and persistence.

Immunity is governed by successful T cell migration, optimized to enable a T cell to fully scan its environment without wasted movement by balancing speed and turning. Here we report that the Arhgef6 RhoGEF (aka alpha-PIX; αPIX; Cool-2), an activator of small GTPases, is required to restrain cell migration speed and cell turning during spontaneous migration on 2D surfaces. In Arhgef6-/- T cells, expression of Arhgef7 (beta-PIX; βPIX; Cool-1), a homolog of Arhgef6, was increased and correlated with defective activation and localization of Rac1 and CDC42 GTPases, respectively. Downstream of Arhgef6, PAK2 (p21-activated kinase 2) and LIMK1 phosphorylation was reduced, leading to increased activation of Cofilin, the actin-severing factor. Consistent with defects in these signaling pathways, Arhgef6-/- T cells displayed abnormal bilobed lamellipodia and migrated faster, turned more, and arrested less than wild-type (WT) T cells. Using pharmacologic inhibition of LIMK1 (LIM domain kinase 1) to induce Cofilin activation in WT T cells, we observed increased migration speed but not increased cell turning. In contrast, inhibition of Cdc42 increased cell turning but not speed. These results suggested that the increased speed of the Arhgef6-/- T cells is due to hyperactive Cofilin while the increased turning may be due to abnormal GTPase activation and recruitment. Together, these findings reveal that Arhgef6 acts as a repressor of T cell speed and turning by limiting actin polymerization and lamellipodia formation.

A phenotypic switch in the dispersal strategy of breast cancer cells selected for metastatic colonization.

An important question in cancer evolution concerns which traits make a cell likely to successfully metastasize. Cell motility phenotypes, mediated by cell shape change, are strong candidates. We experimentally evolved breast cancer cells in vitro for metastatic capability, using selective regimes designed to simulate stages of metastasis, then quantified their motility behaviours using computer vision. All evolved lines showed changes to motility phenotypes, and we have identified a previously unknown density-dependent motility phenotype only seen in cells selected for colonization of decellularized lung tissue. These cells increase their rate of morphological change with an increase in migration speed when local cell density is high. However, when the local cell density is low, we find the opposite relationship: the rate of morphological change decreases with an increase in migration speed. Neither the ancestral population, nor cells selected for their ability to escape or invade extracellular matrix-like environments, displays this dynamic behavioural switch. Our results suggest that cells capable of distant-site colonization may be characterized by dynamic morphological phenotypes and the capacity to respond to the local social environment.

Intravital imaging reveals cell cycle-dependent myogenic cell migration during muscle regeneration

ABSTRACT During muscle regeneration, extracellular signal-regulated kinase (ERK) promotes both proliferation and migration. However, the relationship between proliferation and migration is poorly understood in this context. To elucidate this complex relationship on a physiological level, we established an intravital imaging system for measuring ERK activity, migration speed, and cell-cycle phases in mouse muscle satellite cell-derived myogenic cells. We found that in vivo, ERK is maximally activated in myogenic cells two days after injury, and this is then followed by increases in cell number and motility. With limited effects of ERK activity on migration on an acute timescale, we hypothesized that ERK increases migration speed in the later phase by promoting cell-cycle progression. Our cell-cycle analysis further revealed that in myogenic cells, ERK activity is critical for G1/S transition, and cells migrate more rapidly in S/G2 phase 3 days after injury. Finally, migration speed of myogenic cells was suppressed after CDK1/2—but not CDK1—inhibitor treatment, demonstrating a critical role of CDK2 in myogenic cell migration. Overall, our study demonstrates that in myogenic cells, the ERK-CDK2 axis promotes not only G1/S transition but also migration, thus providing a novel mechanism for efficient muscle regeneration.