Observation of Traction Forces During Galvanotaxis

2013 ◽  
Author(s):  
Nikita Taparia ◽  
Nathan J. Sniadecki
Keyword(s):  
Immune Response ◽  
Wound Healing ◽  
Cell Migration ◽  
Autoimmune Diseases ◽  
Cancer Metastasis ◽  
Critical Role ◽  
Biological Functions ◽  
Traction Forces ◽  
Multicellular Organisms

Cell migration plays a critical role in many biological functions within multicellular organisms such as wound healing, immune response, and embryogenesis. A cell’s inability to migrate can cause severe complications such as inflammatory or autoimmune diseases, defective wound healing or cancer metastasis [1].

The Influence of Polymeric Fiber Stiffness and Alignment on Cytoplasmic Bleb Dynamics and Migration of Glioblastoma Multiforme Cells

2012 ◽  
Author(s):  
Puja Sharma ◽  
Kevin Sheets ◽  
Amrinder S. Nain
Keyword(s):  
Immune Response ◽  
Wound Healing ◽  
Cell Migration ◽  
Glioblastoma Multiforme ◽  
Cancer Progression ◽  
Cancer Metastasis ◽  
Hallmarks Of Cancer ◽  
Multistep Process ◽  
And Migration ◽  
Polymeric Fiber

Cell migration is a tightly regulated phenomenon necessary for regular physiologic processes such as wound healing, immune response, embryonic development, growth, and regeneration [1–3]. Consequences of abnormal migratory behaviors include autoimmune diseases and metastasis during cancer progression [4, 5]. Described as one of the hallmarks of cancer, metastasis is a complex multistep process, and is responsible for 90% of cancer deaths in humans. A better understanding of the process of metastasis is of paramount importance in developing efficient cancer treatment therapies and drugs [6].

scholarly journals Mechanochemical coupling and junctional forces during collective cell migration

2019 ◽  
Author(s):  
J. Bui ◽  
D. E. Conway ◽  
R. L. Heise ◽  
S.H. Weinberg
Keyword(s):  
Cell Migration ◽  
Rho Gtpases ◽  
Cancer Metastasis ◽  
Rho Gtpase ◽  
Critical Role ◽  
Leading Edge ◽  
Collective Cell Migration ◽  
Gtpase Activity ◽  
Modeling Framework ◽  
Cell Cell

ABSTRACTCell migration, a fundamental physiological process in which cells sense and move through their surrounding physical environment, plays a critical role in development and tissue formation, as well as pathological processes, such as cancer metastasis and wound healing. During cell migration, dynamics are governed by the bidirectional interplay between cell-generated mechanical forces and the activity of Rho GTPases, a family of small GTP-binding proteins that regulate actin cytoskeleton assembly and cellular contractility. These interactions are inherently more complex during the collective migration of mechanically coupled cells, due to the additional regulation of cell-cell junctional forces. In this study, we present a minimal modeling framework to simulate the interactions between mechanochemical signaling in individual cells and interactions with cell-cell junctional forces during collective cell migration. We find that migration of individual cells depends on the feedback between mechanical tension and Rho GTPase activity in a biphasic manner. During collective cell migration, waves of Rho GTPase activity mediate mechanical contraction/extension and thus synchronization throughout the tissue. Further, cell-cell junctional forces exhibit distinct spatial patterns during collective cell migration, with larger forces near the leading edge. Larger junctional force magnitudes are associated with faster collective cell migration and larger tissue size. Simulations of heterogeneous tissue migration exhibit a complex dependence on the properties of both leading and trailing cells. Computational predictions demonstrate that collective cell migration depends on both the emergent dynamics and interactions between cellular-level Rho GTPase activity and contractility, and multicellular-level junctional forces.

scholarly journals Fascin limits Myosin activity within Drosophila border cells to control substrate stiffness and promote migration

2021 ◽  
Author(s):  
Maureen C. Lamb ◽  
Chathuri P. Kaluarachchi ◽  
Thiranjeewa I. Lansakara ◽  
Yiling Lan ◽  
Alexei V. Tivanski ◽  
...  
Keyword(s):  
Cell Migration ◽  
Nurse Cell ◽  
Cancer Metastasis ◽  
Critical Role ◽  
Substrate Stiffness ◽  
Cell Stiffness ◽  
Collective Cell Migration ◽  
Border Cells ◽  
Border Cell ◽  
Border Cell Migration

AbstractA key regulator of collective cell migrations, which drive development and cancer metastasis, is substrate stiffness. Increased substrate stiffness promotes migration and is controlled by Myosin. Using Drosophila border cell migration as a model of collective cell migration, we identify, for the first time, that the actin bundling protein Fascin limits Myosin activity in vivo. Loss of Fascin results in: increased activated Myosin on the border cells and their substrate, the nurse cells; decreased border cell Myosin dynamics; and increased nurse cell stiffness as measured by atomic force microscopy. Reducing Myosin restores on-time border cell migration in fascin mutant follicles. Further, Fascin’s actin bundling activity is required to limit Myosin activation. Surprisingly, we find that Fascin regulates Myosin activity in the border cells to control nurse cell stiffness to promote migration. Thus, these data shift the paradigm from a substrate stiffness-centric model of regulating migration, to uncover that collectively migrating cells play a critical role in controlling the mechanical properties of their substrate in order to promote their own migration. This new means of mechanical regulation of migration is likely conserved across contexts and organisms, as Fascin and Myosin are common regulators of cell migration.

scholarly journals Environmental Factors That Influence Stem Cell Migration: An “Electric Field”

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Stephanie N. Iwasa ◽  
Robart Babona-Pilipos ◽  
Cindi M. Morshead
Keyword(s):  
Wound Healing ◽  
Stem Cell ◽  
Cell Migration ◽  
Electric Fields ◽  
Critical Role ◽  
Environmental Stimulus ◽  
Directed Migration ◽  
Stem Cell Migration ◽  
Potential Gradients

Environmental Stimulus of Electric Fields on Stem Cell Migration.The movement of cells in response to electric potential gradients is called galvanotaxis. In vivo galvanotaxis, powered by endogenous electric fields (EFs), plays a critical role during development and wound healing. This review aims to provide a perspective on how stem cells transduce EFs into directed migration and an understanding of the current literature relating to the mechanisms by which cells sense and transduce EFs. We will comment on potential EF-based regenerative medicine therapeutics.

Influence of electrotaxis on cell behaviour

2014 ◽  
Vol 6 (9) ◽  
pp. 817-830 ◽  
Author(s):  
Barbara Cortese ◽  
Ilaria Elena Palamà ◽  
Stefania D'Amone ◽  
Giuseppe Gigli
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Cancer Metastasis ◽  
Cell Behaviour ◽  
Physiological Processes ◽  
Neuron Guidance

Understanding the mechanism of cell migration and interaction with the microenvironment is not only of critical significance to the function and biology of cells, but also has extreme relevance and impact on physiological processes and diseases such as morphogenesis, wound healing, neuron guidance, and cancer metastasis.

scholarly journals Long noncoding RNA ARHGAP5-AS1 inhibits migration of breast cancer cell via stabilizes SMAD7 protein

2020 ◽  
Author(s):  
Chen-Long Wang ◽  
Jing-Chi Li ◽  
Ci-Xiang Zhou ◽  
Cheng-Ning Ma ◽  
Di-Fei Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Noncoding Rna ◽  
Cancer Metastasis ◽  
Critical Role ◽  
Luciferase Reporter ◽  
Functional Study ◽  
Breast Cancer Cell Lines

Abstract Background: Tumor metastasis is the main cause of death from breast cancer patients and cell migration plays a critical role in metastasis. Recent studies have shown long non-coding RNAs (lncRNAs) play an essential role in the initiation and progression of cancer. In the present study, the role of a LncRNA, ARHGAP5-AS1 in breast cancer was investigated.Methods: Bioinformation was analyzed for the expression of ARHGAP5-AS1. qRT-PCR was conducted to verify the expression of ARHGAP5-AS1 in breast cancer specimens. Transwell migration assays and F-actin staining were utilized to estimate cell migration ability. RNA pulldown assays and RNA immunoprecipitation were used to prove the interaction between ARHGAP5-AS1 and SMAD7. Western blot and immunofluorescence imaging were used to examine the protein levels. Dual luciferase reporter assays were performed to evaluate the activation of TGF-β signaling.Results: Compared to MDA-MB-231 cells, the expression of LncRNA ARHGAP5-AS1(NR_027263) was significantly suppressed in its highly metastatic subtype MDA-MB-231-LM2 cells. Functional study showed ARHGAP5-AS1 could inhibit cell migration via suppression of stress fibers in breast cancer cell lines. Afterwards, SMAD7 was further identified to interact with ARHGAP5-AS1 by its PY motif and thus its ubiquitination and degradation was blocked due to reduced interaction with E3 ligase SMURF1 and SMURF2. Moreover, ARHGAP5-AS1 could inhibit TGF-β signaling pathway due to its inhibitory role on SMAD7.Conclusions: Overall, these findings demonstrate that ARHGAP5-AS1 inhibits breast cancer cell migration and could server as a novel biomarker for breast cancer metastasis and a potent target for the treatment in the future.

scholarly journals Critical role of lipid membranes in polarization and migration of cells: a biophysical view

2021 ◽  
Author(s):  
Erich Sackmann ◽  
Motomu Tanaka
Keyword(s):  
Cell Migration ◽  
Lipid Membranes ◽  
Cancer Metastasis ◽  
Membrane Surface ◽  
Critical Role ◽  
Biologically Relevant ◽  
Functional Roles ◽  
And Migration ◽  
Robust Regulation ◽  
Migration Of Cells

AbstractCell migration plays vital roles in many biologically relevant processes such as tissue morphogenesis and cancer metastasis, and it has fascinated biophysicists over the past several decades. However, despite an increasing number of studies highlighting the orchestration of proteins involved in different signaling pathways, the functional roles of lipid membranes have been essentially overlooked. Lipid membranes are generally considered to be a functionless two-dimensional matrix of proteins, although many proteins regulating cell migration gain functions only after they are recruited to the membrane surface and self-organize their functional domains. In this review, we summarize how the logistical recruitment and release of proteins to and from lipid membranes coordinates complex spatiotemporal molecular processes. As predicted from the classical framework of the Smoluchowski equation of diffusion, lipid/protein membranes serve as a 2D reaction hub that contributes to the effective and robust regulation of polarization and migration of cells involving several competing pathways.

scholarly journals Long Noncoding RNA ARHGAP5-AS1 Inhibits Migration of Breast Cancer Cell Via Stabilizes SMAD7 Protein

2020 ◽  
Author(s):  
Chen-Long Wang ◽  
Jing-Chi Li ◽  
Ci-Xiang Zhou ◽  
Cheng-Ning Ma ◽  
Di-Fei Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Noncoding Rna ◽  
Cancer Metastasis ◽  
Critical Role ◽  
Luciferase Reporter ◽  
Functional Study ◽  
Breast Cancer Cell Lines

Abstract Background: Tumor metastasis is the main cause of death from breast cancer patients and cell migration plays a critical role in metastasis. Recent studies have shown long non-coding RNAs (lncRNAs) play an essential role in the initiation and progression of cancer. In the present study, the role of a LncRNA, ARHGAP5-AS1 in breast cancer was investigated. Methods: Bioinformation was analyzed for the expression of ARHGAP5-AS1. qRT-PCR was conducted to verify the expression of ARHGAP5-AS1 in breast cancer specimens. Transwell migration assays and F-actin staining were utilized to estimate cell migration ability. RNA pulldown assays and RNA immunoprecipitation were used to prove the interaction between ARHGAP5-AS1 and SMAD7. Western blot and immunofluorescence imaging were used to examine the protein levels. Dual luciferase reporter assays were performed to evaluate the activation of TGF-β signaling.Results: Compared to MDA-MB-231 cells, the expression of LncRNA ARHGAP5-AS1(NR_027263) was significantly suppressed in its highly metastatic subtype MDA-MB-231-LM2 cells. Functional study showed ARHGAP5-AS1 could inhibit cell migration via suppression of stress fibers in breast cancer cell lines. Afterwards, SMAD7 was further identified to interact with ARHGAP5-AS1 by its PY motif and thus its ubiquitination and degradation was blocked due to reduced interaction with E3 ligase SMURF1 and SMURF2. Moreover, ARHGAP5-AS1 could inhibit TGF-β signaling pathway due to its inhibitory role on SMAD7. Conclusions: Overall, these findings demonstrate that ARHGAP5-AS1 inhibits breast cancer cell migration and could server as a novel biomarker for breast cancer metastasis and a potent target for the treatment in the future.

scholarly journals Galectins in Intra- and Extracellular Vesicles

Biomolecules ◽  
2020 ◽  
Vol 10 (9) ◽  
pp. 1232
Author(s):  
Sebastian Bänfer ◽  
Ralf Jacob
Keyword(s):  
Immune Response ◽  
Cell Migration ◽  
Extracellular Vesicles ◽  
Intracellular Transport ◽  
Cell Communication ◽  
Carbohydrate Binding ◽  
Structural Level ◽  
Transport Pathways ◽  
Membrane Components ◽  
Multicellular Organisms

Carbohydrate-binding galectins are expressed in various tissues of multicellular organisms. They are involved in autophagy, cell migration, immune response, inflammation, intracellular transport, and signaling. In recent years, novel roles of galectin-interaction with membrane components have been characterized, which lead to the formation of vesicles with diverse functions. These vesicles are part of intracellular transport pathways, belong to the cellular degradation machinery, or can be released for cell-to-cell communication. Several characteristics of galectins in the lumen or at the membrane of newly formed vesicular structures are discussed in this review and illustrate the need to fully elucidate their contributions at the molecular and structural level.

scholarly journals PTTG1/securin modulates microtubule nucleation and cell migration

2011 ◽  
Vol 22 (22) ◽  
pp. 4302-4311 ◽  
Author(s):  
Miguel A. Moreno-Mateos ◽  
Águeda G. Espina ◽  
Belén Torres ◽  
María M. Gámez del Estal ◽  
Ana Romero-Franco ◽  
...  
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Cell Types ◽  
Cell Polarization ◽  
Biological Functions ◽  
Microtubule Nucleation ◽  
And Migration ◽  
Different Cell Types ◽  
Transforming Gene

Pituitary tumor transforming gene 1 (PTTG1), also known as securin, has been implicated in many biological functions, including inhibition of sister chromatid separation, DNA repair, organ development, and regulation of the expression and secretion of angiogenic and metastatic factors. Although most of these functions of securin seem to depend on the localization of PTTG1 in the nucleus of the cell, a fraction of the protein has been also detected in the cytoplasm. Here we demonstrate that, in different cell types, a portion of cytoplasmic PTTG1 is associated with the cis face of the Golgi apparatus and that this localization depends on PTTG1 phosphorylation status. In this organelle, PTTG1 forms a complex with proteins involved in microtubule nucleation, including GM130, AKAP450, and γ-tubulin. RNA interference–mediated depletion of PTTG1 produces a delay in centrosomal and noncentrosomal microtubule nucleation. Cells lacking PTTG1 show severe defects in both cell polarization and migration in wound-healing assays. To our knowledge, this is the first study reporting the role of PTTG1 in microtubule nucleation and cell polarization, two processes directly involved in cell migration. We believe that these findings will contribute to understanding the mechanisms underlying PTTG1-mediated biological functions.

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