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Amoeboid mesenchymal

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https://www.readbyqxmd.com/read/29771639/hic-5-expression-is-a-major-indicator-of-cancer-cell-morphology-migration-and-plasticity-in-three-dimensional-matrices
#1
Anushree C Gulvady, Fatemeh Dubois, Nicholas O Deakin, Gregory J Goreczny, Christopher E Turner
The focal adhesion proteins, Hic-5 and Paxillin have been previously identified as key regulators of MDA-MB-231 breast cancer cell migration and morphologic mesenchymal-amoeboid plasticity in three-dimensional extracellular matrices. However, their respective roles in other cancer cell types has not been evaluated. Herein, utilizing 3D cell-derived matrices and fibronectin-coated 1D substrates, we show that across a variety of cancer cell lines, the level of Hic-5 expression serves as the major indicator of the cells primary morphology, plasticity and in vitro invasiveness...
May 17, 2018: Molecular Biology of the Cell
https://www.readbyqxmd.com/read/29760696/podosomes-but-not-the-maturation-status-determine-the-protease-dependent-3d-migration-in-human-dendritic-cells
#2
Céline Cougoule, Claire Lastrucci, Romain Guiet, Rémi Mascarau, Etienne Meunier, Geanncarlo Lugo-Villarino, Olivier Neyrolles, Renaud Poincloux, Isabelle Maridonneau-Parini
Dendritic cells (DC) are professional Antigen-Presenting Cells scattered throughout antigen-exposed tissues and draining lymph nodes, and survey the body for pathogens. Their ability to migrate through tissues, a 3D environment, is essential for an effective immune response. Upon infection, recognition of Pathogen-Associated Molecular Patterns (PAMP) by Toll-like receptors (TLR) triggers DC maturation. Mature DC (mDC) essentially use the protease-independent, ROCK-dependent amoeboid mode in vivo , or in collagen matrices in vitro ...
2018: Frontiers in Immunology
https://www.readbyqxmd.com/read/29615071/mature-and-progenitor-endothelial-cells-perform-angiogenesis-also-under-protease-inhibition-the-amoeboid-angiogenesis
#3
Anastasia Chillà, Francesca Margheri, Alessio Biagioni, Mario Del Rosso, Gabriella Fibbi, Anna Laurenzana
BACKGROUND: Controlling vascular growth is a challenging aim for the inhibition of tumor growth and metastasis. The amoeboid and mesenchymal types of invasiveness are two modes of migration interchangeable in cancer cells: the Rac-dependent mesenchymal migration requires the activity of proteases; the Rho-ROCK-dependent amoeboid motility is protease-independent and has never been described in endothelial cells. METHODS: A cocktail of physiologic inhibitors (Ph-C) of serine-proteases, metallo-proteases and cysteine-proteases, mimicking the physiological environment that cells encounter during their migration within the angiogenesis sites was used to induce amoeboid style migration of Endothelial colony forming cells (ECFCs) and mature endothelial cells (ECs)...
April 3, 2018: Journal of Experimental & Clinical Cancer Research: CR
https://www.readbyqxmd.com/read/29525987/an-in-vitro-system-to-study-the-mesenchymal-to-amoeboid-transition
#4
Aleksandra S Chikina, Antonina Y Alexandrova
During the last few years, significant attention has been given to the plasticity of cell migration, i.e., the ability of individual cell to switch between different motility modes, in particular between mesenchymal and amoeboid motilities. This phenomenon is called the mesenchymal-to-amoeboid transition (MAT). Such a plasticity of cell migration is a mechanism, by which cancer cells can adapt their migration mode to different microenvironments and thus it may promote tumor dissemination. It was shown that interventions at certain regulatory points of mesenchymal motility as well as alterations of environmental conditions can trigger MAT...
2018: Methods in Molecular Biology
https://www.readbyqxmd.com/read/29517849/bone-marrow-derived-mesenchymal-stem-cells-promote-invasiveness-and-transendothelial-migration-of-osteosarcoma-cells-via-a-mesenchymal-to-amoeboid-transition
#5
Laura Pietrovito, Angela Leo, Valentina Gori, Matteo Lulli, Matteo Parri, Valentina Becherucci, Luisa Piccini, Franco Bambi, Maria Letizia Taddei, Paola Chiarugi
There is growing evidence to suggest that bone marrow-derived mesenchymal stem cells (BM-MSCs) are key players in tumour stroma. Here, we investigated the cross-talk between BM-MSCs and osteosarcoma (OS) cells. We revealed a strong tropism of BM-MSCs towards these tumour cells and identified monocyte chemoattractant protein (MCP)-1, growth-regulated oncogene (GRO)-α and transforming growth factor (TGF)-β1 as pivotal factors for BM-MSC chemotaxis. Once in contact with OS cells, BM-MSCs trans-differentiate into cancer-associated fibroblasts, further increasing MCP-1, GRO-α, interleukin (IL)-6 and IL-8 levels in the tumour microenvironment...
May 2018: Molecular Oncology
https://www.readbyqxmd.com/read/29379163/c-src-activity-is-differentially-required-by-cancer-cell-motility-modes
#6
Jeremy S Logue, Alexander X Cartagena-Rivera, Richard S Chadwick
Cancer cell migration requires that cells respond and adapt to their surroundings. In the absence of extracellular matrix cues, cancer cells will undergo a mesenchymal to ameboid transition, whereas a highly confining space will trigger a switch to "leader bleb-based" migration. To identify oncogenic signaling pathways mediating these transitions, we undertook a targeted screen using clinically useful inhibitors. Elevated Src activity was found to change actin and focal adhesion dynamics, whereas inhibiting Src triggered focal adhesion disassembly and blebbing...
April 2018: Oncogene
https://www.readbyqxmd.com/read/29274473/tyro3-mediated-phosphorylation-of-actn4-at-tyrosines-is-fak-dependent-and-decreases-susceptibility-to-cleavage-by-m-calpain
#7
Hanshuang Shao, Anna Wang, Douglas Lauffenburger, Alan Wells
Tyro3, a member of TAM receptor tyrosine kinase family, has been implicated in the regulation of melanoma progression and survival. In this study, we sought the molecular mechanism of Tyro3 effects avoiding endogenous background by overexpression of Tyro3 in fibroblasts that have negligible levels of Tyro3. This introduction triggers the tyrosyl-phosphorylation of ACTN4, a member of actin binding protein family involved in motility, a behavior critical for invasive progression, as shown by siRNA to Tyro3 limiting melanoma cell migration and invasion...
February 2018: International Journal of Biochemistry & Cell Biology
https://www.readbyqxmd.com/read/29196116/contact-guidance-diversity-in-rotationally-aligned-collagen-matrices
#8
Jacob A M Nuhn, Anai M Perez, Ian C Schneider
Cancer cell metastasis is responsible for approximately 90% of deaths related to cancer. The migration of cancer cells away from the primary tumor and into healthy tissue is driven in part by contact guidance, or directed migration in response to aligned extracellular matrix. While contact guidance has been a focus of many studies, much of this research has explored environments that present 2D contact guidance structures. Contact guidance environments in 3D more closely resemble in vivo conditions and model cell-ECM interactions better than 2D environments...
January 15, 2018: Acta Biomaterialia
https://www.readbyqxmd.com/read/29136112/local-production-of-tenascin-c-acts-as-a-trigger-for-monocyte-macrophage-recruitment-that-provokes-cardiac-dysfunction
#9
Dounia Abbadi, Fanny Laroumanie, Mathilde Bizou, Joffrey Pozzo, Danièle Daviaud, Christine Delage, Denis Calise, Fréderique Gaits-Iacovoni, Marianne Dutaur, Florence Tortosa, Edith Renaud-Gabardos, Victorine Douin-Echinard, Anne-Catherine Prats, Jerome Roncalli, Angelo Parini, Nathalie Pizzinat
Aims: Tenascin-C (TNC) is an endogenous danger signal molecule strongly associated with inflammatory diseases and with poor outcome in patients with cardiomyopathies. Its function within pathological cardiac tissue during pressure overload remains poorly understood. Methods and results: We showed that TNC accumulates after 1 week of transverse aortic constriction (TAC) in the heart of 12-week-old male mice. By cross bone marrow transplantation experiments, we determined that TNC deposition relied on cardiac cells and not on haematopoietic cells...
January 1, 2018: Cardiovascular Research
https://www.readbyqxmd.com/read/29115617/three-dimensional-hydrogel-is-suitable-for-targeted-investigation-of-amoeboid-migration-of-glioma-cells
#10
Yubao Huang, Luqing Tong, Li Yi, Chen Zhang, Long Hai, Tao Li, Shengping Yu, Wei Wang, Zhennan Tao, Haiwen Ma, Peidong Liu, Yang Xie, Xuejun Yang
Glioblastoma (GBM) invasion and migration are key biological behaviors leading to refractoriness to current therapies and infiltration into the non‑tumor brain parenchyma. GBM cell migration is strongly dependent on tumor architecture in vivo, which is absent in traditional two‑dimensional (2D) monolayer culture. The present study applied a three‑dimensional (3D) hydrogel model to rebuild the tumor architecture in vitro. Treatment with NSC23766, a specific inhibitor of Ras‑related C3 botulinum toxin substrate 1 (Rac1), inhibited the mesenchymal invasiveness however triggered the amoeboid motility called mesenchymal‑amoeboid transition (MAT)...
January 2018: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28972134/live-imaging-reveals-distinct-modes-of-neutrophil-and-macrophage-migration-within-interstitial-tissues
#11
Francisco Barros-Becker, Pui-Ying Lam, Robert Fisher, Anna Huttenlocher
Cell motility is required for diverse processes during immunity and inflammation. Classically, leukocyte motility is defined as an amoeboid type of migration, however some leukocytes, like macrophages, also employ a more mesenchymal mode of migration. Here, we sought to characterize the mechanisms that regulate neutrophil and macrophage migration in vivo by using real-time imaging of leukocyte motility within interstitial tissues in zebrafish larvae. Neutrophils displayed a rounded morphology and rapid protease-independent motility, lacked defined paxillin puncta, and had persistent rearward polarization of stable F-actin and the microtubule network...
November 15, 2017: Journal of Cell Science
https://www.readbyqxmd.com/read/28835679/amoeboid-mesenchymal-migration-plasticity-promotes-invasion-only-in-complex-heterogeneous-microenvironments
#12
Katrin Talkenberger, Elisabetta Ada Cavalcanti-Adam, Anja Voss-Böhme, Andreas Deutsch
During tissue invasion individual tumor cells exhibit two interconvertible migration modes, namely mesenchymal and amoeboid migration. The cellular microenvironment triggers the switch between both modes, thereby allowing adaptation to dynamic conditions. It is, however, unclear if this amoeboid-mesenchymal migration plasticity contributes to a more effective tumor invasion. We address this question with a mathematical model, where the amoeboid-mesenchymal migration plasticity is regulated in response to local extracellular matrix resistance...
August 23, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28650698/the-rock-isoforms-differentially-regulate-the-morphological-characteristics-of-carcinoma-cells
#13
Rachel J Jerrell, Mitchell J Leih, Aron Parekh
Rho-associated kinase (ROCK) activity drives cell migration via actomyosin contractility. During invasion, individual cancer cells can transition between two modes of migration, mesenchymal and amoeboid. Changes in ROCK activity can cause a switch between these migration phenotypes which are defined by distinct morphologies. However, recent studies have shown that the ROCK isoforms are not functionally redundant as previously thought. Therefore, it is unclear whether the ROCK isoforms play different roles in regulating migration phenotypes...
June 26, 2017: Small GTPases
https://www.readbyqxmd.com/read/28487031/hmec-1-adopt-the-mixed-amoeboid-mesenchymal-migration-type-during-endmt
#14
Jakub Kryczka, Patrycja Przygodzka, Helena Bogusz, Joanna Boncela
The contribution of endothelial cells to scar and fibrotic tissue formation is undisputedly connected to their ability to undergo the endothelial-to-mesenchymal transition (EndMT) towards fibroblast phenotype-resembling cells. The migration model of fibroblasts and fibroblast-resembling cells is still not fully understood. It may be either a Rho/ROCK-independent, an integrin- and MMP-correlated ECM degradation-dependent, a mesenchymal model or Rho/ROCK-dependent, integrin adhesion- and MMP activity-independent, an amoeboid model...
June 2017: European Journal of Cell Biology
https://www.readbyqxmd.com/read/28353134/ontogeny-of-ramified-cd45-cells-in-chicken-embryo-and-their-contribution-to-bursal-secretory-dendritic-cells
#15
Dávid Dóra, Nóra Fejszák, Allan M Goldstein, Krisztina Minkó, Nándor Nagy
Embryonic tissues contain highly ramified stellate-shaped cells expressing CD45 and MHC II antigens but their origin and immunophenotype are unknown. Using staged avian embryos and cell-type-specific antibodies, we establish a detailed spatiotemporal ontogeny of cells that express CD45, the earliest marker of hematopoietic stem cells in the chick. CD45 immunostaining marks three distinct embryonic cell populations: round, ramified and amoeboid cells. The round and ramified CD45+ cells appear first in yolk-sac blood islands before the onset of circulation...
May 2017: Cell and Tissue Research
https://www.readbyqxmd.com/read/28235899/dual-targeting-of-mesenchymal-and-amoeboid-motility-hinders-metastatic-behavior
#16
Brandon C Jones, Laura C Kelley, Yuriy V Loskutov, Kristina M Marinak, Varvara K Kozyreva, Matthew B Smolkin, Elena N Pugacheva
Commonly upregulated in human cancers, the scaffolding protein NEDD9/HEF1 is a known regulator of mesenchymal migration and cancer cell plasticity. However, the functional role of NEDD9 as a regulator of different migration/invasion modes in the context of breast cancer metastasis is currently unknown. Here, it is reported that NEDD9 is necessary for both mesenchymal and amoeboid individual cell migration/invasion in triple-negative breast cancer (TNBC). NEDD9 deficiency results in acquisition of the amoeboid morphology, but severely limits all types of cell motility...
June 2017: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/28166248/characterization-of-three-dimensional-cancer-cell-migration-in-mixed-collagen-matrigel-scaffolds-using-microfluidics-and-image-analysis
#17
María Anguiano, Carlos Castilla, Martin Maška, Cristina Ederra, Rafael Peláez, Xabier Morales, Gorka Muñoz-Arrieta, Maite Mujika, Michal Kozubek, Arrate Muñoz-Barrutia, Ana Rouzaut, Sergio Arana, José Manuel Garcia-Aznar, Carlos Ortiz-de-Solorzano
Microfluidic devices are becoming mainstream tools to recapitulate in vitro the behavior of cells and tissues. In this study, we use microfluidic devices filled with hydrogels of mixed collagen-Matrigel composition to study the migration of lung cancer cells under different cancer invasion microenvironments. We present the design of the microfluidic device, characterize the hydrogels morphologically and mechanically and use quantitative image analysis to measure the migration of H1299 lung adenocarcinoma cancer cells in different experimental conditions...
2017: PloS One
https://www.readbyqxmd.com/read/28115158/mdia2-and-cxcl12-cxcr4-chemokine-signaling-intersect-to-drive-tumor-cell-amoeboid-morphological-transitions
#18
Meghan M Wyse, Silvia Goicoechea, Rafael Garcia-Mata, Andrea L Nestor-Kalinoski, Kathryn M Eisenmann
Morphological plasticity in response to environmental cues in migrating cancer cells requires F-actin cytoskeletal rearrangements. Conserved formin family proteins play critical roles in cell shape, tumor cell motility, invasion and metastasis, in part, through assembly of non-branched actin filaments. Diaphanous-related formin-2 (mDia2/Diaph3/Drf3/Dia) regulates mesenchymal-to-amoeboid morphological conversions and non-apoptotic blebbing in tumor cells by interacting with its inhibitor diaphanous-interacting protein (DIP), and disrupting cortical F-actin assembly and bundling...
March 4, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28089517/hypoxia-induces-a-hif-1-dependent-transition-from-collective-to-amoeboid-dissemination-in-epithelial-cancer-cells
#19
Steffi Lehmann, Veronika Te Boekhorst, Julia Odenthal, Roberta Bianchi, Sjoerd van Helvert, Kristian Ikenberg, Olga Ilina, Szymon Stoma, Jael Xandry, Liying Jiang, Reidar Grenman, Markus Rudin, Peter Friedl
Cancer metastases arise from a multi-step process that requires metastasizing tumor cells to adapt to signaling input from varying tissue environments [1]. As an early metastatic event, cancer cell dissemination occurs through different migration programs, including multicellular, collective, and single-cell mesenchymal or amoeboid migration [2-4]. Migration modes can interconvert based on changes in cell adhesion, cytoskeletal mechanotransduction [5], and/or proteolysis [6], most likely under the control of transcriptional programs such as the epithelial-to-mesenchymal transition (EMT) [7, 8]...
February 6, 2017: Current Biology: CB
https://www.readbyqxmd.com/read/27941881/the-nadph-oxidase-nox4-represses-epithelial-to-amoeboid-transition-and-efficient-tumour-dissemination
#20
E Crosas-Molist, E Bertran, I Rodriguez-Hernandez, C Herraiz, G Cantelli, À Fabra, V Sanz-Moreno, I Fabregat
Epithelial to mesenchymal transition is a common event during tumour dissemination. However, direct epithelial to amoeboid transition has not been characterized to date. Here we provide evidence that cells from hepatocellular carcinoma (HCC), a highly metastatic cancer, undergo epithelial to amoeboid transition in physiological environments, such as organoids or three-dimensional complex matrices. Furthermore, the NADPH oxidase NOX4 inhibits this transition and therefore suppresses efficient amoeboid bleb-based invasion...
May 25, 2017: Oncogene
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