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Relevant bibliographies by topics / Amoeboid motility

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Academic literature on the topic 'Amoeboid motility'

Author: Grafiati

Published: 14 March 2023

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Journal articles on the topic "Amoeboid motility"

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Leo, Angela, Erica Pranzini, Laura Pietrovito, Elisa Pardella, Matteo Parri, Paolo Cirri, Gennaro Bruno, et al. "Claisened Hexafluoro Inhibits Metastatic Spreading of Amoeboid Melanoma Cells." Cancers 13, no. 14 (July 15, 2021): 3551. http://dx.doi.org/10.3390/cancers13143551.

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Metastatic melanoma is characterized by poor prognosis and a low free-survival rate. Thanks to their high plasticity, melanoma cells are able to migrate exploiting different cell motility strategies, such as the rounded/amoeboid-type motility and the elongated/mesenchymal-type motility. In particular, the amoeboid motility strongly contributes to the dissemination of highly invasive melanoma cells and no treatment targeting this process is currently available for clinical application. Here, we tested Claisened Hexafluoro as a novel inhibitor of the amoeboid motility. Reported data demonstrate that Claisened Hexafluoro specifically inhibits melanoma cells moving through amoeboid motility by deregulating mitochondrial activity and activating the AMPK signaling. Moreover, Claisened Hexafluoro is able to interfere with the adhesion abilities and the stemness features of melanoma cells, thus decreasing the in vivo metastatic process. This evidence may contribute to pave the way for future possible therapeutic applications of Claisened Hexafluoro to counteract metastatic melanoma dissemination.

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Pietrovito, Laura, Giuseppina Comito, Matteo Parri, Elisa Giannoni, Paola Chiarugi, and Maria Letizia Taddei. "Zoledronic Acid Inhibits the RhoA-mediated Amoeboid Motility of Prostate Cancer Cells." Current Cancer Drug Targets 19, no. 10 (December 23, 2019): 807–16. http://dx.doi.org/10.2174/1568009619666190115142858.

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Background:The bisphosphonate Zoledronic acid (ZA) is a potent osteoclast inhibitor currently used in the clinic to reduce osteoporosis and cancer-induced osteolysis. Moreover, ZA exerts an anti-tumor effect in several tumors. Despite this evidence, the relevance of ZA in prostate cancer (PCa) is not completely understood.Objective:To investigate the effect of ZA administration on the invasive properties of PC3 cells, which are characterised by RhoA-dependent amoeboid motility.Methods:The effect of ZA administration on the in vitro invasive properties of PC3 cells was evaluated by cell migration in 3D collagen matrices, immunofluorescence and Boyden assays or transendothelial migration. Lung retention and colonization assays were performed to assess the efficacy of ZA administration in vivo.Results:PC3 cells are characterised by RhoA-dependent amoeboid motility. We now report a clear inhibition of in vitro PC3 cell invasion and RhoA activity upon ZA treatment. Moreover, to confirm a specific role of ZA in the inhibition of amoeboid motility of PC3 cells, we demonstrate that ZA interferes only partially with PC3 cells showing a mesenchymal phenotype due to both treatment with conditioned medium of cancer associated fibroblasts or to the acquisition of chemoresistance. Furthermore, we demonstrate that ZA impairs adhesion to endothelial cells and the trans-endothelial cell migration, two essential properties characterising amoeboid motility and PC3 metastatic dissemination. In vivo experiments prove the ability of ZA to inhibit the metastatic process of PC3 cells as shown by the decrease in lung colonization.Conclusion:This study demonstrates that ZA inhibits Rho-dependent amoeboid motility of PC3 cells, thus suggesting ZA as a potential therapy to impede the metastatic dissemination of PC3 cells.

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Klemm, Lucas C., Ryan A. Denu, Laurel E. Hind, Briana L. Rocha-Gregg, Mark E. Burkard, and Anna Huttenlocher. "Centriole and Golgi microtubule nucleation are dispensable for the migration of human neutrophil-like cells." Molecular Biology of the Cell 32, no. 17 (August 15, 2021): 1545–56. http://dx.doi.org/10.1091/mbc.e21-02-0060.

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Callan-Jones, A. C., and R. Voituriez. "Active gel model of amoeboid cell motility." New Journal of Physics 15, no. 2 (February 18, 2013): 025022. http://dx.doi.org/10.1088/1367-2630/15/2/025022.

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Peretz-Soroka, Hagit, Reuven Tirosh, Jolly Hipolito, Erwin Huebner, Murray Alexander, Jason Fiege, and Francis Lin. "A bioenergetic mechanism for amoeboid-like cell motility profiles tested in a microfluidic electrotaxis assay." Integrative Biology 9, no. 11 (2017): 844–56. http://dx.doi.org/10.1039/c7ib00086c.

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Dalal, Swapnil, Alexander Farutin, and Chaouqi Misbah. "Amoeboid swimming in a compliant channel." Soft Matter 16, no. 6 (2020): 1599–613. http://dx.doi.org/10.1039/c9sm01689a.

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We studied influence of elasticity of surrounding environment on cell motility by numerically investigating effects of wall flexibility and channel confinement on flow dynamics of amoeboid swimming in compliant channel.

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Saito, Koji, Yuta Ozawa, Keisuke Hibino, and Yasutaka Ohta. "FilGAP, a Rho/Rho-associated protein kinase–regulated GTPase-activating protein for Rac, controls tumor cell migration." Molecular Biology of the Cell 23, no. 24 (December 15, 2012): 4739–50. http://dx.doi.org/10.1091/mbc.e12-04-0310.

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Tumor cells exhibit two interconvertible modes of cell motility referred to as mesenchymal and amoeboid migration. Mesenchymal mode is characterized by elongated morphology that requires high GTPase Rac activation, whereas amoeboid mode is dependent on actomyosin contractility induced by Rho/Rho-associated protein kinase (ROCK) signaling. While elongated morphology is driven by Rac-induced protrusion at the leading edge, how Rho/ROCK signaling controls amoeboid movement is not well understood. We identified FilGAP, a Rac GTPase-activating protein (GAP), as a mediator of Rho/ROCK-dependent amoeboid movement of carcinoma cells. We show that depletion of endogenous FilGAP in carcinoma cells induced highly elongated mesenchymal morphology. Conversely, forced expression of FilGAP induced a round/amoeboid morphology that requires Rho/ROCK-dependent phosphorylation of FilGAP. Moreover, depletion of FilGAP impaired breast cancer cell invasion through extracellular matrices and reduced tumor cell extravasation in vivo. Thus phosphorylation of FilGAP by ROCK appears to promote amoeboid morphology of carcinoma cells, and FilGAP contributes to tumor invasion.

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Copos, Calina A., Robert D. Guy, Sam Walcott, Juan Carlos del Alamo, and Alex Mogilner. "Mechanosensitive Adhesion Explains Stepping Motility in Amoeboid Cells." Biophysical Journal 112, no. 3 (February 2017): 433a. http://dx.doi.org/10.1016/j.bpj.2016.11.2315.

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Bullock, Timothy L., Airlie J. McCoy, Helen M. Kent, Thomas M. Roberts, and Murray Stewart. "Structural basis for amoeboid motility in nematode sperm." Nature Structural Biology 5, no. 3 (March 1998): 184–89. http://dx.doi.org/10.1038/nsb0398-184.

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Copos, Calina A., Sam Walcott, Juan C. del Álamo, Effie Bastounis, Alex Mogilner, and Robert D. Guy. "Mechanosensitive Adhesion Explains Stepping Motility in Amoeboid Cells." Biophysical Journal 112, no. 12 (June 2017): 2672–82. http://dx.doi.org/10.1016/j.bpj.2017.04.033.

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Dissertations / Theses on the topic "Amoeboid motility"

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Zanchi, Roberto. "The involvement of the endocytic cycle in amoeboid cell motility." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608458.

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Leo, Angela. "The study of cell motility and plasticity in cancer: the role of the crosstalk between BM-MSCs and tumor in osteosarcoma progression and Claisened Hexafluoro as potential inhibitor of amoeboid motility in metastatic melanoma." Doctoral thesis, Università di Siena, 2021. http://hdl.handle.net/11365/1128636.

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Part 1 Growing evidence suggest that bone marrow-derived mesenchymal stem cells (BM-MSCs) are key players in tumor stroma. Here, we investigated the cross-talk between BM-MSCs and osteosarcoma (OS) cells in tumor progression. We revealed a strong tropism of BM-MSCs towards these tumor 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 tumor microenvironment. These cytokines promote mesenchymal to amoeboid transition (MAT), driven by activation of the small GTPase RhoA, in OS cells, as illustrated by the in vitro assay and live imaging. The outcome is a significant increase of aggressiveness in OS cells in terms of motility, invasiveness and trans-endothelial migration. In keeping with their enhanced trans-endothelial migration abilities, OS cells stimulated by BM-MSCs also sustain migration and invasion. Thus, BM-MSC recruitment to the OS site and the consequent cytokine-induced MAT are crucial events in OS malignancy. Part 2 Metastatic melanoma is one of the most aggressive and lethal malignancies with a poor prognosis. Melanoma cells are able to migrate using different types of cell motility such as the rounded/amoeboid-type motility and the elongated/mesenchymal-type motility thanks to their high plasticity. Really several data underline the crucial role of amoeboid motility in the dissemination process of highly metastatic melanoma cells. Thus, targeting this process could be a promising strategy to prevent the metastatic spreading of melanoma cells. Claisened Hexafluoro is a chemical analog of Honokiol (HKL), a biphenolic compound derived from Magnolia officinalis which has antitumoral and antimetastatic effect in numerous cancers, including melanoma. Starting from these evidence, here we tested Claisened Hexafluoro on human metastatic melanoma cells, as an inhibitor of amoeboid motility. Data here reported demonstrate that Claisened Hexafluoro, impairing mitochondrial activity and affecting AMP-activated protein kinase (AMPK) signaling, strongly inhibits amoeboid motility and many steps of the disseminating process in vitro as well as in vivo, confirming its possible future application to fight metastatic spreading of melanoma cells.

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Lewis, Owen Leslie. "Mathematical Investigation of Hydrodynamic Contributions to Amoeboid Cell Motility in Physarum polycephalum." Thesis, University of California, Davis, 2015. http://pqdtopen.proquest.com/#viewpdf?dispub=3685252.

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In this work, we investigate the role of intracellular fluid flow in the migration of Physarum polycephalum. We develop two distinct models. Initially, we model the intracellular space of a physarum plasmodium as a peristaltic chamber. We derive a PDE relating the deformation of the chamber boundary and the flux of fluid along the chamber center line. We then solve this PDE for two distinct boundary deformations and evaluate the characteristic stress associated with the peristaltic flow. We compare the derived stress, as well as the relative phase of the deformation and flow waves, with values seen in experiments. Second, we develop a poro-elastic model of the interior of physarum that accounts for cytoskeletal structure, as well as adhesive interactions with the substrate. We develop this model within a framework similar to the Immersed Boundary method, which readily allows for computer simulation. We then use this model to simulate cell crawling across a range of parameters that characterize the coordination of adhesion to the substrate. We identify a spatio-temporal form of adhesion coordination that is consistent with experiments. We also show that this form is both efficient and robust, when compared to similar forms of adhesion coordination.

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Ingram, Mark Edward. "Whole Skin Locomotion Inspired by Amoeboid Motility Mechanisms: Mechanics of the Concentric Solid Tube Model." Thesis, Virginia Tech, 2006. http://hdl.handle.net/10919/35100.

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As the technology of robotics intelligence advances, and new application areas for mobile robots increase, the need for alternative fundamental locomotion mechanisms for robots that allow them to maneuver into complex unstructured terrain becomes critical. In this research we present a novel locomotion mechanism for mobile robots inspired by the motility mechanism of certain single celled organisms such as amoebae. Whole Skin Locomotion (WSL), as we call it, works by way of an elongated toroid which turns itself inside out in a single continuous motion, effectively generating the overall motion of the cytoplasmic streaming ectoplasmic tube in amoebae. This research presents the preliminary analytical study towards the design and development of the novel WSL mechanism. In this thesis we first investigate how amoebas move, then discuss how this motion can be replicated. By applying the biological theories of amoeboid motility mechanisms, different actuation models for WSL are developed including the Fluid Filled Toroid (FFT) and Concentric Solid Tube (CST) models. Then, a quasi-static force analysis is performed for the CST model and parametric studies for design, including power efficiency and force transition characteristics, are presented.
Master of Science

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D'Alessandro, Joseph. "Collective regulation of the amoeboid motility : the role of short and long-range interactions in vegetative Dictyostelium discoideum." Thesis, Lyon, 2016. http://www.theses.fr/2016LYSE1039/document.

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La motilité cellulaire est fondamentale dans de nombreux processus physiologiques, qu’ils soient normaux ou pathologiques. Cependant, bien que ces derniers impliquent la plupart du temps de nombreuses cellules se mouvant en même temps, les effets des interactions entre cellules sur leur dynamique, à la fois individuelle et collective, restent assez mal connu. Dans cette thèse, j’ai utilisé Dictyostelium discoideum à l’état végétatif pour étudier cette régulation collective de la motilité. Je me suis principalement appuyé sur une analyse minutieuse de nombreuses trajectoires cellulaires dans des situations variées pour (i) caractériser un facteur sécrété qui régule négativement la motilité cellulaire (nature chimique, voie de signalisation, dynamique de sécrétion et de réponse) et (ii) analyser et modéliser quantitativement la dynamique d’étalement de colonie cellulaires de forme, dimension et densité contrôlées. Je décris enfin un phénomène d’agrégation dynamique observé lorsque les cellules sont placées à haute densité dans un milieu nutritif
Cell motility is fundamental in many physiological, either normal or pathological, phenomena. Yet, although these most often involve several cells moving at the same time, how the interactions between cells affect both individual and collective dynamics remains a poorly understood question. In this thesis, I used vegetative Dictyostelium discoideum cells as a model to study this collective regulation of the motility. I relied mainly on the thorough analysis of numerous cell trajectories in various situations to (i) characterise a secreted factor used to down-regulate the cells’ motility (biochemical nature, response pathway, secretion and response dynamics) and (ii) quantitatively analyse and model the dynamics of spreading cell colonies of controlled initial shape, size and density. Last, I describe a dynamic aggregation phenomenon that occurs when the cells are seeded at high density in a nutrient-rich medium

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Wyse, Meghan M. "CXCL12 Mediated Regulation of the Cytoskeletal Regulator mDia2 Formin Induces Amoeboid Conversions and Cellular Plasticity in Migrating Human Breast Carcinoma Cells." University of Toledo / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1404042854.

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Kulawiak, Dirk Alexander [Verfasser], Harald [Akademischer Betreuer] Engel, Harald [Gutachter] Engel, Markus [Gutachter] Bär, and Carsten [Gutachter] Beta. "Physical minimal models of amoeboid cell motility / Dirk Alexander Kulawiak ; Gutachter: Harald Engel, Markus Bär, Carsten Beta ; Betreuer: Harald Engel." Berlin : Technische Universität Berlin, 2017. http://d-nb.info/1156010403/34.

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Nègre, Paulin. "Mécanismes de motilité et guidage sous flux des leucocytes humains." Thesis, Aix-Marseille, 2018. http://www.theses.fr/2018AIXM0747/document.

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La capacité des leucocytes à se déplacer dans tout l’organisme est indispensable pour une réponse immunitaire rapide et efficace. Leur migration, dite amiboïde, est caractérisée par une vitesse importante (10-20 μm/min) et une grande adaptabilité face aux divers environnements qu’ils rencontrent, qu’ils soient bidimensionnels comme la paroi luminale endothéliale ou tridimensionnels (3D) comme les tissus. Telle qu'actuellement décrite, la migration amiboïde requiert de l’adhésion ou de la friction avec un support solide. Nous avons ici montré que les lymphocytes T effecteurs sont capables de nager sans interaction avec un support solide. Le mécanisme de propulsion est basé sur le flux rétrograde d’actine qui entraine une brosse protéique de molécules transmembranaires liées au cytosquelette entrant en interaction avec le medium. Par ailleurs, lors de leur migration sur la surface luminale des parois endothéliales, les leucocytes sont soumis à un flux important et s’orientent par rapport au flux via des mécanismes mal déterminés. Nous avons montré que l’orientation des lymphocytes et des neutrophiles respectivement dans le sens ou à contresens d’un flux peut s’expliquer sans détection moléculaire du stress hydrodynamique. Le lamellipode pour les neutrophiles et l’uropode pour les lymphocytes est non-adhérent et s’oriente dans le flux comme une girouette dans le vent. La polarisation avant-arrière réaligne l’ensemble de la cellule dans le même sens que l’extrémité orientée par le flux. Le mécanotactisme des leucocytes sous flux repose ainsi sur des mécanismes passifs, c’est-à-dire sans mécanotransduction
A fast and efficient immunity response needs leukocytes’ability to migrate within the entire organism. Their migration, called amoeboid, is characterized by a high speed (10-20 μm.min-1) and a great adaptability to move through various environment, either two-dimensional as luminal endothelial surface or tri-dimensional (3D) environment as tissue. Since the observation of leukocytes migrating without adhesion through solid 3D medium, amoeboid migration is described as requiring either adhesion or friction with solid support to permit motility. We showed here that effector T lymphocytes are able to swim without any interaction with solid substrate. Propulsion is based on actin retrograde flow coupled with transmembrane proteins linked to cytoskeleton (like integrins) which drag a brush of polymeric molecules in interaction with the medium. Furthermore, cell guidance is required for many crucial functions as organism growth or immune system. However, when crawling on luminal endothelial surfaces, cells are exposed to blood flow and they robustly orient either with or against the flow with unknown mechanisms. We showed that lymphocytes and neutrophils flow orientation can be explain without any molecular flow sensor of shear stress. Lamellipodium for neutrophils and uropod for lymphocytes is non-adherent and orients in the direction of flow like a wind vane. Front-rear cell polarization aligns the axis of the whole cell with the non-adherent pole oriented by flow. Flow mechanotaxis of leukocytes relies on passive mechanisms without mechanotransduction

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Buttery, Shawnna Marie Roberts Thomas M. "Characterization of the cytosolic proteins involved in the amoeboid motility of ascaris sperm." 2003. http://etd.lib.fsu.edu/theses/available/etd-08192004-100416.

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Thesis (Ph. D.)--Florida State University, 2003.
Advisor: Dr. Thomas M. Roberts, Florida State University, College of Arts and Sciences, Department of Biological Science. Title and description from dissertation home page (viewed Aug. 23, 2004). Includes bibliographical references.

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Book chapters on the topic "Amoeboid motility"

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Shimmen, T. "Mechanisms of Cytoplasmic Streaming and Amoeboid Movement." In Muscle Contraction and Cell Motility, 172–205. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-76927-6_6.

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Italiano, Joseph E., Murray Stewart, and Thomas M. Roberts. "How the assembly dynamics of the nematode major sperm protein generate amoeboid cell motility." In International Review of Cytology, 1–34. Elsevier, 2001. http://dx.doi.org/10.1016/s0074-7696(01)02002-2.

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Fukui, Yoshio. "Toward a New Concept of Cell Motility: Cytoskeletal Dynamics in Amoeboid Movement and Cell Division." In International Review of Cytology, 85–127. Elsevier, 1993. http://dx.doi.org/10.1016/s0074-7696(08)61514-4.

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Maynard Smith, John, and Eors Szathmary. "The origin of eukaryotes." In The Major Transitions in Evolution. Oxford University Press, 1997. http://dx.doi.org/10.1093/oso/9780198502944.003.0012.

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The basic structures of a bacterial and a eukaryotic cell are shown in Fig. 8.1. The differences whose origins call for an explanation are as follows: • The bacterial cell has a rigid outer cell wall, usually made of the peptidoglycan, murein. In eukaryotes, the rigid cell wall is not universal, and cell shape is maintained primarily by an internal cytoskeleton of filaments and microtubules. • Eukaryotic cells have a complex system of internal membranes, including the nuclear envelope, endoplasmic reticulum and lysosomes. • Bacteria have a single circular chromosome, attached to the rigid outer cell wall. In eukaryotes, linear chromosomes are contained within a nuclear envelope, which separates transcription from translation: communication between nucleus and cytoplasm is via pores in the nuclear envelope. • Eukaryotes have a complex cytoskeleton. The actomyosin system powers cell division, phagocytosis, amoeboid motion and the overall contractility to resist osmotic swelling. Microtubules and the associated motor proteins (kinesin, dynein and dynamin) ensure the accurate segregation of chromosomes in mitosis, ciliary motility and the movement of transport vesicles. Intermediate filaments form the structural basis for the association of the endomembranes and nuclear-pore complexes with the chromatin to form the nuclear envelope, while other intermediate filaments help to anchor the nucleus in the cytoplasm. One crucial difference between prokaryotes and most eukaryotes has been omitted from Fig. 8.1: this is the presence of mitochondria, and, in plants and algae, of chloroplasts. The reason for the omission is that, on the scenario for eukaryote origins that seems to us most plausible, these intracellular organelles originated later in time than the structures shown in the figure. The differences between these cell types justifies the recognition of two empires of life (above the kingdom level): Bacteria and Eukaryota (Cavalier-Smith, 199la; Table 8.1). (It is interesting that this taxonomic rank was recognized by Linnaeus.) Within each of the empires, there are two major categories: Bacteria consist of the kingdoms Eubacteria and Archaebacteria, and Eukaryota are divided into the superkingdoms Archaezoa and Metakaryota. The justification for these divisions is as follows. The Archaebacteria, in contrast to the Eubacteria, never have murein cell walls, and their single cell membrane contains isoprenoidal ether rather than acyl ester lipids.

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Conference papers on the topic "Amoeboid motility"

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Xiong, Yuan, and Pablo A. Iglesias. "Automated characterization of amoeboid motility." In 2009 43rd Annual Conference on Information Sciences and Systems (CISS). IEEE, 2009. http://dx.doi.org/10.1109/ciss.2009.5054747.

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Ingram, Mark, and Dennis Hong. "Whole Skin Locomotion Inspired by Amoeboid Motility Mechanisms." In ASME 2005 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2005. http://dx.doi.org/10.1115/detc2005-85419.

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In this paper, we present a novel locomotion mechanism for mobile robots inspired by the motility mechanisms of single celled organisms that use cytoplasmic streaming to generate pseudopods for locomotion. The Whole Skin Locomotion, as we call it, works by way of an elongated toroid which turns itself inside out in a single continuous motion, effectively generating the overall motion of the cytoplasmic streaming ectoplasmic tube in amoebae. With an elastic membrane or a mesh of links acting as its outer skin, the robot can easily squeeze between obstacles or under a collapsed ceiling and move forward using all of its contact surfaces for traction, or even squeeze itself through holes with diameters smaller than its nominal width by actively changing its cross section diameter making this the ideal locomotion method for search and rescue robots that need to traverse over or under rubble, or for applications where a robot needs to move in and maneuver itself into tight spaces such as for robotic endoscopes. This paper summarizes the many existing theories of amoeboid motility mechanisms, and examines how these can be applied on a macro scale as a novel mobile robot locomotion concept. Four locomotion mechanism models are presented with preliminary experiments and their results, demonstrating the feasibility of the whole skin locomotion strategy.

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Wyse, Meghan M., Andrea L. Nestor-Kalinoski, and Kathryn M. Eisenmann. "Abstract C50: CXCL12-triggered amoeboid cell motility is mediated through a RhoA-directed signaling hub." In Abstracts: AACR Special Conference on Tumor Invasion and Metastasis - January 20-23, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tim2013-c50.

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Eisenmann, Kathryn. "Abstract LB-270: Regulation of the cortical actin cytoskeleton and amoeboid motility through the mDia2 formin;DIP complex." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-lb-270.

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Mohamed, Islam, Ahmed Moahmed, Mennatallah Abdelkader, Alaaeldin Saleh, and Ala-Eddin Al-Moustafa. "Elaeagnus Angustifolia: a Promising Medicinal Plant for Cancer Theraby." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0124.

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Introduction: Elaeagnus angustifolia (EA) is a medicinal plant that has been used for centuries in treating many human diseases, in the Middle East, including fever, amoebic dysentery, gastrointestinal problems. However, the effect of EA plant extract on human cancer progression especially oral malignancy has not been investigated yet. Thus, first we examined the effect of EA flower extract on angiogenesis in ovo, and on selected parameters in human oral cancer cells. Materials and methods: Chorioallantoic membranes (CAMs) of chicken embryos at 3-7 days of incubation were used to assess the effect EAflower plant extract on angiogenesis. Meanwhile, cell proliferation, soft agar, cell cycle, cell invasion and cell wounding assays were performed to explore the outcome of EA plant extract on FaDu and SCC25 oral cancer cell lines. On the other hand, western blot analysis was carried out to evaluate E-cadherin and Erk1/Erk2 expression and activation, respectively, in FaDu and SCC25 under the effect of EA extract. Results: Our data show that EA extract inhibits cell proliferation and colony formation, in addition to the initiation of Scell cycle arrest and reductionof G1/G2 phases. In parallel, EA extract provokes differentiation to an epithelial phenotype “mesenchymal-epithelial transition: MET” which is the opposite of “epithelial-mesenchymal transition, EMT”: an important event in cell invasion and metastasis. Thus, EA extract causes a dramatic decrease in cell motility and invasion abilities of FaDu and SCC25 cancer cells in comparison with their controls. These changes are accompanied by an up-regulation of E-cadherin expression. The molecular pathway analysis of the EA flower extract reveals that it can inhibit the phosphorylation of Erk1/Erk2, which could be behind the inhibition of angiogenesis, the initiation of MET event and the overexpression of E-cadherin. Conclusions: Our findings indicate that EA plant extract can downgrade human oral cancer progression by the inhibition of angiogenesis and cell invasion via Erk1/Erk2 signaling pathways.

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