ERK signaling promotes cell motility by inducing the localization of myosin 1E to lamellipodial tips

Tanimura, Susumu; Hashizume, Junya; Arichika, Naoya; Watanabe, Kazushi; Ohyama, Kaname; Takeda, Kohsuke; Kohno, Michiaki

doi:10.1083/jcb.201503123

Cited by 30 publications

(58 citation statements)

References 34 publications

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“…A miR‐125b binding site was identified in the 3ʹUTR of rat Myo1e (Figure A). Myo1e is an actin‐dependent molecular motor previously reported to play a role in lamellipodium extension and subsequent cell migration . A dual luciferase assay was therefore performed with WT and mutant (MUT) constructs of the Myo1e 3′UTR in VSMCs transfected with miR‐125b mimic or inhibitor (Figure B).…”

Section: Resultsmentioning

confidence: 99%

“…Myo1e is an actin-dependent molecular motor previously reported to play a role in lamellipodium extension and subsequent cell migration. 26 Focal adhesion kinase has been reported to play a role in the proliferation and migration of aortic smooth muscle cells, and the regulation of smooth muscle cell recruitment during blood vessel morphogenesis. [28][29][30] Myo1e has previously been reported to induce FAK phosphorylation and FAK kinase activity.…”

Section: Exosomal Mir-125b Suppresses Vsmc Proliferation and Migratmentioning

confidence: 99%

“…Myosin‐1E (Myo1e) is an actin‐dependent molecular motor whose translocation is essential for lamellipodium extension and subsequent cellular motility and cell migration . Heim et al reported that Myo1e binds to the FERM domain of focal adhesion kinase (FAK), activating FAK and inducing Y397 phosphorylation.…”

Section: Introductionmentioning

confidence: 99%

“…Myosin-1E (Myo1e) is an actin-dependent molecular motor whose translocation is essential for lamellipodium extension and subsequent cellular motility and cell migration. 26 Heim et al 27…”

Section: Introductionmentioning

confidence: 99%

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Exosomes from mesenchymal stem cells expressing miR‐125b inhibit neointimal hyperplasia via myosin IE

Wang

Gao

Yue

et al. 2018

J Cellular Molecular Medi

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Intercellular communication between mesenchymal stem cells (MSCs) and their target cells in the perivascular environment is modulated by exosomes derived from MSCs. However, the potential role of exosome‐mediated microRNA transfer in neointimal hyperplasia remains to be investigated. To evaluate the effects of MSC‐derived exosomes (MSC‐Exo) on neointimal hyperplasia, their effects upon vascular smooth muscle cell (VSMC) growth in vitro and neointimal hyperplasia in vivo were assessed in a model of balloon‐induced vascular injury. Our results showed that MSC‐Exo were internalised by VSMCs and inhibited proliferation and migration in vitro. Further analysis revealed that miR‐125b was enriched in MSC‐Exo, and repressed the expression of myosin 1E (Myo1e) by targeting its 3ʹ untranslated region. Additionally, MSC‐Exo and exosomally transferred miR‐125b repressed Myo1e expression and suppressed VSMC proliferation and migration and neointimal hyperplasia in vivo. In summary, our findings revealed that MSC‐Exo can transfer miR‐125b to VSMCs and inhibit VSMC proliferation and migration in vitro and neointimal hyperplasia in vivo by repressing Myo1e, indicating that miR‐125b may be a therapeutic target in the treatment of vascular diseases.

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Section: Resultsmentioning

confidence: 99%

Section: Exosomal Mir-125b Suppresses Vsmc Proliferation and Migratmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…Myosin-1E (Myo1e) is an actin-dependent molecular motor whose translocation is essential for lamellipodium extension and subsequent cellular motility and cell migration. 26 Heim et al 27…”

Section: Introductionmentioning

confidence: 99%

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Exosomes from mesenchymal stem cells expressing miR‐125b inhibit neointimal hyperplasia via myosin IE

Wang

Gao

Yue

et al. 2018

J Cellular Molecular Medi

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“…in the formation of actin filaments. This role for myosin1e is further supported by two additional studies showing that lamellipodia formation and stability is impaired in myosin1e-deficient cells (Gupta et al, 2013;Tanimura et al, 2016). It is also important to note that cells expressing a variant of myosin1e lacking the SH3 domain fail to form mature focal adhesions (Gupta et al, 2013).…”

Section: Discussionmentioning

confidence: 88%

LSP1-myosin1e bi-molecular complex regulates focal adhesion dynamics and cell migration

Schaeringer

Maxeiner

Schalla

et al. 2020

Preprint

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Telephone: +49 241 8085248Running head: LSP1-myosin1e complex regulates cell migration. Abstract Several cytoskeleton-associated proteins and signalling pathways work in concert to regulate actin cytoskeleton remodelling, cell adhesion and migration. We have recently demonstrated that the bi-molecular complex between the leukocyte-specific protein 1 (LSP1) and myosin1e controls actin cytoskeleton remodelling during phagocytosis. In this study, we show that LSP1 down regulation severely impairs cell migration, lamellipodia formation and focal adhesion dynamics in macrophages.Inhibition of the interaction between LSP1 and myosin1e also impairs these processes resulting in poorly motile cells, which are characterised by few and small lamellipodia.Furthermore, cells in which LSP1-myosin1e interaction is inhibited are typically associated with inefficient focal adhesion turnover. Collectively, our findings show that the LSP1-myosin1e bimolecular complex plays a pivotal role in the regulation of actin cytoskeleton remodelling and focal adhesion dynamics required for cell migration.

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Myosin 1e deficiency affects migration of 4T1 breast cancer cells

Garone,

Chase,

Zhang

et al. 2023

Cytoskeleton

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Metastasis of breast cancer cells to distant tissue sites is responsible for the majority of deaths associated with breast cancer. Previously we have examined the role of class I myosin motor protein, myosin 1e (myo1e), in cancer metastasis using the Mouse Mammary Tumor Virus‐Polyoma Middle T Antigen (MMTV‐PyMT) mouse model. Mice deficient in myo1e formed tumors with a more differentiated phenotype relative to the wild‐type mice and formed no detectable lung metastases. In the current study, we investigated how the absence of myo1e affects cell migration and invasion in vitro, using the highly invasive and migratory breast cancer cell line, 4T1. 4T1 cells deficient in myo1e exhibited an altered morphology and slower rates of migration in the wound‐healing and transwell migration assays compared to the WT 4T1 cells. While integrin trafficking and Golgi reorientation did not appear to be altered upon myo1e loss, we observed lower rates of focal adhesion disassembly in myo1e‐deficient cells, which could help explain the cell migration defect.

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ERK signaling promotes cell motility by inducing the localization of myosin 1E to lamellipodial tips

Cited by 30 publications

References 34 publications

Exosomes from mesenchymal stem cells expressing miR‐125b inhibit neointimal hyperplasia via myosin IE

Exosomes from mesenchymal stem cells expressing miR‐125b inhibit neointimal hyperplasia via myosin IE

LSP1-myosin1e bi-molecular complex regulates focal adhesion dynamics and cell migration

Myosin 1e deficiency affects migration of 4T1 breast cancer cells

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