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Journal articles on the topic 'Cell migration strategies'

Author: Grafiati

Published: 4 June 2021

Last updated: 8 February 2022

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1

Kameritsch, Petra, and Jörg Renkawitz. "Principles of Leukocyte Migration Strategies." Trends in Cell Biology 30, no. 10 (2020): 818–32. http://dx.doi.org/10.1016/j.tcb.2020.06.007.

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Krummel, Matthew F., Frederic Bartumeus, and Audrey Gérard. "T cell migration, search strategies and mechanisms." Nature Reviews Immunology 16, no. 3 (2016): 193–201. http://dx.doi.org/10.1038/nri.2015.16.

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Kummerow, Carsten, Hélène Lyrmann, Marc Neef, et al. "Modeling Killer Cell Migration and Search Strategies." Biophysical Journal 104, no. 2 (2013): 320a. http://dx.doi.org/10.1016/j.bpj.2012.11.1773.

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4

Hatzikirou, H., K. Böttger, and A. Deutsch. "Model-based Comparison of Cell Density-dependent Cell Migration Strategies." Mathematical Modelling of Natural Phenomena 10, no. 1 (2015): 94–107. http://dx.doi.org/10.1051/mmnp/201510105.

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5

Painter, K. J. "Modelling cell migration strategies in the extracellular matrix." Journal of Mathematical Biology 58, no. 4-5 (2008): 511–43. http://dx.doi.org/10.1007/s00285-008-0217-8.

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6

Baeyens, Audrey, Victoria Fang, Cynthia Chen, and Susan R. Schwab. "Exit Strategies: S1P Signaling and T Cell Migration." Trends in Immunology 36, no. 12 (2015): 778–87. http://dx.doi.org/10.1016/j.it.2015.10.005.

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7

Isabelle Comte, Phuong B. Tran, and Francis G. Szele. "Techniques and Strategies to Analyze Neural Progenitor Cell Migration." Current Pharmaceutical Biotechnology 8, no. 3 (2007): 177–85. http://dx.doi.org/10.2174/138920107780906513.

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Li, Gaigai, Yang Hu, Yanfang Chen, and Zhouping Tang. "Strategies to Improve the Migration of Mesenchymal Stromal Cells in Cell Therapy." Translational Neuroscience and Clinics 3, no. 3 (2017): 159–75. http://dx.doi.org/10.18679/cn11-6030_r.2017.025.

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Mesenchymal stromal/stem cells (MSCs) are multipotent cells under consideration as a potential new therapy for a variety of inflammatory diseases including certain neurological disorders. It is generally thought that the efficacy of cell therapy in attenuating damage after ischemia, inflammation, or injury depends on the quantity of transplanted cells recruited to the target tissue. However, only a small number of systematically infused MSCs can effectively migrate to target sites, which significantly decreases the efficacy of exogenous cell-based therapy. In this review, we discuss specific f

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Li, Gaigai, Gaigai Li, Yang Hu, et al. "Strategies to improve the migration of mesenchymal stromal cells in cell therapy." Translational Neuroscience and Clinics 3, no. 3 (2017): 159–75. http://dx.doi.org/10.18679/cn11-6030/r.2017.025.

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10

Friedl, P., E. B. Bröcker, and K. S. Zänker. "Integrins, Cell Matrix Interactions and Cell Migration Strategies: Fundamental Differences in Leukocytes and Tumor Cells." Cell Adhesion and Communication 6, no. 2-3 (1998): 225–36. http://dx.doi.org/10.3109/15419069809004478.

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11

Friedl, Peter, Eva-B. Bröcker, and K. S. Zänker. "Integrins, cell matrix interactions and cell migration strategies: Fundamental differences in leukocytes and tumor cells." Journal of Dermatological Science 16 (March 1998): S124. http://dx.doi.org/10.1016/s0923-1811(98)83738-9.

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Richardson, Brian E., and Ruth Lehmann. "Mechanisms guiding primordial germ cell migration: strategies from different organisms." Nature Reviews Molecular Cell Biology 11, no. 1 (2010): 37–49. http://dx.doi.org/10.1038/nrm2815.

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13

Hung, Wei-Chien, Shih-Hsun Chen, Colin D. Paul, et al. "Distinct signaling mechanisms regulate migration in unconfined versus confined spaces." Journal of Cell Biology 202, no. 5 (2013): 807–24. http://dx.doi.org/10.1083/jcb.201302132.

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Using a microchannel assay, we demonstrate that cells adopt distinct signaling strategies to modulate cell migration in different physical microenvironments. We studied α4β1 integrin–mediated signaling, which regulates cell migration pertinent to embryonic development, leukocyte trafficking, and melanoma invasion. We show that α4β1 integrin promotes cell migration through both unconfined and confined spaces. However, unlike unconfined (2D) migration, which depends on enhanced Rac1 activity achieved by preventing α4/paxillin binding, confined migration requires myosin II–driven contractility, w

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14

Millarte, Valentina, and Hesso Farhan. "The Golgi in Cell Migration: Regulation by Signal Transduction and Its Implications for Cancer Cell Metastasis." Scientific World Journal 2012 (2012): 1–11. http://dx.doi.org/10.1100/2012/498278.

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Migration and invasion are fundamental features of metastatic cancer cells. The Golgi apparatus, an organelle involved in posttranslational modification and sorting of proteins, is widely accepted to regulate directional cell migration. In addition, mounting evidence suggests that the Golgi is a hub for different signaling pathways. In this paper we will give an overview on how polarized secretion and microtubule nucleation at the Golgi regulate directional cell migration. We will review different signaling pathways that signal to and from the Golgi. Finally, we will discuss how these signalin

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15

Zhu, Jie, and Alex Mogilner. "Comparison of cell migration mechanical strategies in three-dimensional matrices: a computational study." Interface Focus 6, no. 5 (2016): 20160040. http://dx.doi.org/10.1098/rsfs.2016.0040.

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Cell migration on a two-dimensional flat surface has been extensively studied and is generally characterized by a front-protrusion–rear-contraction process. In a three-dimensional (3D) environment, on the other hand, cells adopt multiple migration strategies depending on the cell type and the properties of the extracellular matrix (ECM). By using computer simulations, we find that these migration strategies can be classified by various spatial–temporal dynamics of actin protrusion, actin–myosin contraction and actin–ECM adhesion. We demonstrate that if we include or exclude proteolysis of ECM,

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16

Wolf, Katarina, Irina Mazo, Harry Leung, et al. "Compensation mechanism in tumor cell migration." Journal of Cell Biology 160, no. 2 (2003): 267–77. http://dx.doi.org/10.1083/jcb.200209006.

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Invasive tumor dissemination in vitro and in vivo involves the proteolytic degradation of ECM barriers. This process, however, is only incompletely attenuated by protease inhibitor–based treatment, suggesting the existence of migratory compensation strategies. In three-dimensional collagen matrices, spindle-shaped proteolytically potent HT-1080 fibrosarcoma and MDA-MB-231 carcinoma cells exhibited a constitutive mesenchymal-type movement including the coclustering of β1 integrins and MT1–matrix metalloproteinase (MMP) at fiber bindings sites and the generation of tube-like proteolytic degradat

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17

Hopper, Niina, John Wardale, Daniel Howard, Roger Brooks, Neil Rushton, and Frances Henson. "Peripheral Blood Derived Mononuclear Cells Enhance the Migration and Chondrogenic Differentiation of Multipotent Mesenchymal Stromal Cells." Stem Cells International 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/323454.

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A major challenge in cartilage repair is the lack of chondrogenic cells migrating from healthy tissue into damaged areas and strategies to promote this should be developed. The aim of this study was to evaluate the effect of peripheral blood derived mononuclear cell (PBMC) stimulation on mesenchymal stromal cells (MSCs) derived from the infrapatellar fat pad of human OA knee. Cell migration was measured using an xCELLigence electronic migration chamber system in combination with scratch assays. Gene expression was quantified with stem cell PCR arrays and validated using quantitative real-time

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Kang, Sung Keun, Il Seob Shin, Myung Soon Ko, Jung Youn Jo, and Jeong Chan Ra. "Journey of Mesenchymal Stem Cells for Homing: Strategies to Enhance Efficacy and Safety of Stem Cell Therapy." Stem Cells International 2012 (2012): 1–11. http://dx.doi.org/10.1155/2012/342968.

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Human mesenchymal stem cells (MSCs) communicate with other cells in the human body and appear to “home” to areas of injury in response to signals of cellular damage, known as homing signals. This review of the state of current research on homing of MSCs suggests that favorable cellular conditions and thein vivoenvironment facilitate and are required for the migration of MSCs to the site of insult or injuryin vivo. We review the current understanding of MSC migration and discuss strategies for enhancing both the environmental and cellular conditions that give rise to effective homing of MSCs. T

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19

Ellis, Vincent, and Gillian Murphy. "Cellular strategies for proteolytic targeting during migration and invasion." FEBS Letters 506, no. 1 (2001): 1–5. http://dx.doi.org/10.1016/s0014-5793(01)02845-9.

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20

Friedl, Peter, and Katarina Wolf. "Proteolytic and non-proteolytic migration of tumour cells and leucocytes." Biochemical Society Symposia 70 (September 1, 2003): 277–85. http://dx.doi.org/10.1042/bss0700277.

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The migration of different cell types, such as leucocytes and tumour cells, involves cellular strategies to overcome the physical resistance of three-dimensional tissue networks, including proteolytic degradation of extracellular matrix (ECM) components. High-resolution live-cell imaging techniques have recently provided structural and biochemical insight into the differential use of matrix-degrading enzymes in the migration processes of different cell types within the three-dimensional ECM. Proteolytic migration is achieved by slow-moving cells, such as fibroblasts and mesenchymally moving tu

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21

Carey, Shawn P., Aniqua Rahman, Casey M. Kraning-Rush, et al. "Comparative mechanisms of cancer cell migration through 3D matrix and physiological microtracks." American Journal of Physiology-Cell Physiology 308, no. 6 (2015): C436—C447. http://dx.doi.org/10.1152/ajpcell.00225.2014.

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Tumor cell invasion through the stromal extracellular matrix (ECM) is a key feature of cancer metastasis, and understanding the cellular mechanisms of invasive migration is critical to the development of effective diagnostic and therapeutic strategies. Since cancer cell migration is highly adaptable to physiochemical properties of the ECM, it is critical to define these migration mechanisms in a context-specific manner. Although extensive work has characterized cancer cell migration in two- and three-dimensional (3D) matrix environments, the migration program employed by cells to move through

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22

Friedl, Peter, Kurt S. Zänker, and Eva-B. Bröcker. "Cell migration strategies in 3-D extracellular matrix: Differences in morphology, cell matrix interactions, and integrin function." Microscopy Research and Technique 43, no. 5 (1998): 369–78. http://dx.doi.org/10.1002/(sici)1097-0029(19981201)43:5<369::aid-jemt3>3.0.co;2-6.

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23

Piacentino, Michael L., Yuwei Li, and Marianne E. Bronner. "Epithelial-to-mesenchymal transition and different migration strategies as viewed from the neural crest." Current Opinion in Cell Biology 66 (October 2020): 43–50. http://dx.doi.org/10.1016/j.ceb.2020.05.001.

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24

Su, Peihong, Ye Tian, Chaofei Yang, et al. "Mesenchymal Stem Cell Migration during Bone Formation and Bone Diseases Therapy." International Journal of Molecular Sciences 19, no. 8 (2018): 2343. http://dx.doi.org/10.3390/ijms19082343.

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During bone modeling, remodeling, and bone fracture repair, mesenchymal stem cells (MSCs) differentiate into chondrocyte or osteoblast to comply bone formation and regeneration. As multipotent stem cells, MSCs were used to treat bone diseases during the past several decades. However, most of these implications just focused on promoting MSC differentiation. Furthermore, cell migration is also a key issue for bone formation and bone diseases treatment. Abnormal MSC migration could cause different kinds of bone diseases, including osteoporosis. Additionally, for bone disease treatment, the migrat

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25

Collins, Tyler A., Benjamin M. Yeoman, and Parag Katira. "To lead or to herd: optimal strategies for 3D collective migration of cell clusters." Biomechanics and Modeling in Mechanobiology 19, no. 5 (2020): 1551–64. http://dx.doi.org/10.1007/s10237-020-01290-y.

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26

Mrass, Paulus, Hajime Takano, Lai Guan Ng, et al. "Random migration precedes stable target cell interactions of tumor-infiltrating T cells." Journal of Experimental Medicine 203, no. 12 (2006): 2749–61. http://dx.doi.org/10.1084/jem.20060710.

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The tumor microenvironment is composed of an intricate mixture of tumor and host-derived cells that engage in a continuous interplay. T cells are particularly important in this context as they may recognize tumor-associated antigens and induce tumor regression. However, the precise identity of cells targeted by tumor-infiltrating T lymphocytes (TILs) as well as the kinetics and anatomy of TIL-target cell interactions within tumors are incompletely understood. Furthermore, the spatiotemporal conditions of TIL locomotion through the tumor stroma, as a prerequisite for establishing contact with t

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27

Yang, Long, Guangning Zhao, Fan Wang, Chunchang Li, and Xiangzhong Wang. "Hypoxia-Regulated miR-146a Targets Cell Adhesion Molecule 2 to Promote Proliferation, Migration, and Invasion of Clear Cell Renal Cell Carcinoma." Cellular Physiology and Biochemistry 49, no. 3 (2018): 920–31. http://dx.doi.org/10.1159/000493224.

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Background/Aims: miR-146a has recently been shown to promote cell proliferation, migration, and invasion in many cancers, but the role of miR-146a in clear cell renal cell carcinoma (ccRCC) remains unclear. Methods: Reverse transcription quantitative PCR (RT-qPCR) was performed to investigate the mRNA expression of miR-146a and CADM2 in ccRCC tissues. The luciferase reporter assay, Western blotting, and ChIP assay were carried out to explore the promoter and the transcription factor of miR-146a. Moreover, the effect of miR-146a and CADM2 on ccRCC cells was explored using methyl thiazolyl tetra

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28

Witko, Tomasz, Daria Solarz, Karolina Feliksiak, Katarzyna Haraźna, Zenon Rajfur, and Maciej Guzik. "Insights into In Vitro Wound Closure on Two Biopolyesters—Polylactide and Polyhydroxyoctanoate." Materials 13, no. 12 (2020): 2793. http://dx.doi.org/10.3390/ma13122793.

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Two bio-based polymers have been compared in this study, namely: polylactide (PLA) and polyhydroxyoctanoate (PHO). Due to their properties such as biocompatibility, and biointegrity they are considered to be valuable materials for medical purposes, i.e., creating scaffolds or wound dressings. Presented biopolymers were investigated for their impact on cellular migration strategies of mouse embryonic fibroblasts (MEF) 3T3 cell line. Advanced microscopic techniques, including confocal microscopy and immunofluorescent protocols, enabled the thorough analysis of the cell shape and migration. Appli

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de los Reyes V, Aurelio A., Eunok Jung, and Yangjin Kim. "Optimal control strategies of eradicating invisible glioblastoma cells after conventional surgery." Journal of The Royal Society Interface 12, no. 106 (2015): 20141392. http://dx.doi.org/10.1098/rsif.2014.1392.

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Glioblastoma, the most aggressive type of brain cancer, has median survival time of 1 year after diagnosis. It is characterized by alternating modes of rapid proliferation and aggressive invasion in response to metabolic stress in the microenvironment. A particular microRNA, miR-451, and its downstream signalling molecules, AMPK complex, are known to be key determinants in switching cell fate. These components form a core control system determining a balance between cell growth and migration which is regulated by fluctuating glucose levels in the microenvironment. An important factor from the

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Friedl, Peter, and Eva-Bettina Bröker. "T Cell Migration in Three-dimensional Extracellular Matrix: Guidance by Polarity and Sensations." Developmental Immunology 7, no. 2-4 (2000): 249–66. http://dx.doi.org/10.1155/2000/56473.

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The locomotion of T lymphocytes within 3-D extracellular matrix (ECM) is a highly dynamic and flexible process following the principles of ameboid movement. Ameboid motility is characterized by a polarized yet simple cell shape allowing high speed, rapid directional oscillations, and low affinity interactions to the substrate that are coupled to a low degree of cytoskeletal organization lacking discrete focal contacts. At the onset of T cell migration, a default program, here described as migration-associated polarization, is initiated, resulting in the polar redistribution of cell surface rec

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Xiao, Wen, Ning Lou, Hailong Ruan, et al. "Mir-144-3p Promotes Cell Proliferation, Metastasis, Sunitinib Resistance in Clear Cell Renal Cell Carcinoma by Downregulating ARID1A." Cellular Physiology and Biochemistry 43, no. 6 (2017): 2420–33. http://dx.doi.org/10.1159/000484395.

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Background/Aims: We previously performed microRNA (miRNA) microarray to identify effective indicators of clear cell renal cell carcinoma (ccRCC) tissue samples and preoperative/postoperative plasma in which we identified miR-144-3p as an oncomiRNA. However, the molecular mechanism of miR-144-3p remains unclear. This study aims to explore the roles of miR-144-3p in the invasion, migration and Sunitinib-resistance in ccRCC and to elucidate the underlying mechanisms. Methods: Gain and loss of function approaches were used to investigate the cell proliferation, cycle distribution, clonogenicity, m

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Masoumi, Katarzyna Chmielarska, Xiaoli Huang, Wondossen Sime та ін. "Integrin α10-Antibodies Reduce Glioblastoma Tumor Growth and Cell Migration". Cancers 13, № 5 (2021): 1184. http://dx.doi.org/10.3390/cancers13051184.

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Glioblastoma (GB) is the most common and the most aggressive form of brain tumor in adults, which currently lacks efficient treatment strategies. In this study, we investigated the therapeutic effect of function-blocking antibodies targeting integrin α10β1 on patient-derived-GB cell lines in vitro and in vivo. The in vitro studies demonstrated significant inhibiting effects of the integrin α10 antibodies on the adhesion, migration, proliferation, and sphere formation of GB cells. In a xenograft mouse model, the effect of the antibodies on tumor growth was investigated in luciferase-labeled and

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Wang, Sitong, Fanwu Wu, Bin Ye, et al. "Effects of Xuefu Zhuyu Decoction on Cell Migration and Ocular Tumor Invasion in Drosophila." BioMed Research International 2020 (April 25, 2020): 1–13. http://dx.doi.org/10.1155/2020/5463652.

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Xuefu Zhuyu Decoction (XFZYD), a Traditional Chinese Medicine (TCM) decoction mainly for treating blood stasis syndrome, has been widely investigated and applied in clinic and in laboratory. XFZYD contains 11 herbs and has been identified to promoting blood circulation to remove blood stasis for cardiovascular disease. Meanwhile, blood stasis is directly related to malignant tumor according to TCM basic theory. However, the effects of XFZYD on tumor metastasis and the underlying mechanisms are still largely unknown. Here, we employed well-established Drosophila cell migration and tumor invasio

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Cui, Guoce, and Xia Kong. "DNA Methyltransferase 1 Affects Proliferation and Migration of Colorectal Cancer Cells by Regulating Ras Association Domain Family 1 Methylation." Materials Express 9, no. 8 (2019): 949–55. http://dx.doi.org/10.1166/mex.2019.1571.

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The effects of DNMT1 on human colorectal cancer cell proliferation and apoptosis as well as the possible underlying mechanisms were investigated. SW480 cells were treated with the DNA methyltransferase inhibitor 5-AZA-CdR. qRT-PCR was used to analyze mRNA expression, whereas protein expression was evaluated by western blotting. Cell growth, migration, and invasion were measured by MTT, transwell migration, and wound healing assays, respectively. Cell morphology was observed using hematoxylin and eosin (H&E) staining. 5-AZA-CdR treatment inhibited DNMT1 expression in colorectal cancer cells

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Dastmalchi, Farhad, Aida Karachi, Changlin Yang, et al. "EXTH-15. INCREASING THE TRAFFICKING OF DENDRITIC CELLS VIA CXC CHEMOKINE SIGNALING PATHWAY LEADS TO IMPROVED ANTI-TUMOR EFFICACY OF DENDRITIC CELL VACCINES." Neuro-Oncology 21, Supplement_6 (2019): vi85. http://dx.doi.org/10.1093/neuonc/noz175.349.

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Abstract Dendritic cell (DC) vaccine efficacy is directly related to the efficiency of DC migration to the lymph node after delivery to the patient. In this research we discovered increasing cell migration by utilizing sarcosine improved anti-tumor efficacy. We hypothesized that sarcosine induced cell migration was due to chemokine or cytokine signaling. METHODS To generate DC vaccines, DCs were harvested from bone marrow of wild type C57BL/6 mice and electroporated with OVA-mRNA. Human DCs were isolated from PBMCs. DCs were treated with sarcosine at 20mM. OT-I T cells were isolated from trans

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36

Liu, Haijun, Xiaoniu Dai, Yusi Cheng, et al. "MCPIP1 mediates silica-induced cell migration in human pulmonary fibroblasts." American Journal of Physiology-Lung Cellular and Molecular Physiology 310, no. 2 (2016): L121—L132. http://dx.doi.org/10.1152/ajplung.00278.2015.

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Silicosis is a systemic disease caused by inhaling silicon dioxide (SiO2). Phagocytosis of SiO2 in the lungs initiates an inflammatory cascade that results in fibroblast proliferation and migration followed by fibrosis. According to previous data from our laboratory, monocyte chemotactic protein-1 (MCP-1) plays a critical role in fibroblast proliferation and migration in conventional two-dimensional (2D) monolayer cultures. The present study aimed to explore the downstream cascade of MCP-1 in both 2D and three-dimensional (3D) cell culture models of silicosis. Experiments using primary culture

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Casalou, Cristina, Alexandra Faustino, Fernanda Silva, et al. "Arl13b Regulates Breast Cancer Cell Migration and Invasion by Controlling Integrin-Mediated Signaling." Cancers 11, no. 10 (2019): 1461. http://dx.doi.org/10.3390/cancers11101461.

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Breast cancer is the first cause of cancer-related mortality among women worldwide, according to the most recent estimates. This mortality is mainly caused by the tumors’ ability to form metastases. Cancer cell migration and invasion are essential for metastasis and rely on the interplay between actin cytoskeleton remodeling and cell adhesion. Therefore, understanding the mechanisms by which cancer cell invasion is controlled may provide new strategies to impair cancer progression. We investigated the role of the ADP-ribosylation factor (Arf)-like (Arl) protein Arl13b in breast cancer cell mig

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38

Zheng, Ping-Pin, Lies-Anne Severijnen, Marcel van der Weiden, Rob Willemsen, and Johan M. Kros. "Cell proliferation and migration are mutually exclusive cellular phenomena in vivo: Implications for cancer therapeutic strategies." Cell Cycle 8, no. 6 (2009): 950–51. http://dx.doi.org/10.4161/cc.8.6.7851.

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39

Hideshima, Teru, and Kenneth C. Anderson. "Signaling Pathway Mediating Myeloma Cell Growth and Survival." Cancers 13, no. 2 (2021): 216. http://dx.doi.org/10.3390/cancers13020216.

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The multiple myeloma (MM) bone marrow (BM) microenvironment consists of different types of accessory cells. Both soluble factors (i.e., cytokines) secreted from these cells and adhesion of MM cells to these cells play crucial roles in activation of intracellular signaling pathways mediating MM cell growth, survival, migration, and drug resistance. Importantly, there is crosstalk between the signaling pathways, increasing the complexity of signal transduction networks in MM cells in the BM microenvironment, highlighting the requirement for combination treatment strategies to blocking multiple s

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Hideshima, Teru, and Kenneth C. Anderson. "Signaling Pathway Mediating Myeloma Cell Growth and Survival." Cancers 13, no. 2 (2021): 216. http://dx.doi.org/10.3390/cancers13020216.

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The multiple myeloma (MM) bone marrow (BM) microenvironment consists of different types of accessory cells. Both soluble factors (i.e., cytokines) secreted from these cells and adhesion of MM cells to these cells play crucial roles in activation of intracellular signaling pathways mediating MM cell growth, survival, migration, and drug resistance. Importantly, there is crosstalk between the signaling pathways, increasing the complexity of signal transduction networks in MM cells in the BM microenvironment, highlighting the requirement for combination treatment strategies to blocking multiple s

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She, Chunhua, Marine Potez, JongMyung Kim, and James Liu. "BSCI-06. Phage display biopanning identifies Amot regulating cell motility in brain metastasis-initiating cells." Neuro-Oncology Advances 3, Supplement_3 (2021): iii2. http://dx.doi.org/10.1093/noajnl/vdab071.005.

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Abstract Objective Metastatic brain tumors (MBTs) are the most common type of malignant brain tumors. Due to the deviation of MBTs from the parental tumors, the effective therapies for primary tumors often are not working in brain metastases. Even more new intracranial lesions were developed though the primary lesion was controlled. The occurrence of brain metastasis-initiating cells (BMICs) suggested the possibility of its spread intracranially. Here we aimed to explore the biological behavior in cell motility of BMICs and understand the potential mechanisms. Methods In vitro and in vivo phag

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Alberch, P., and E. Kollar. "Strategies of head development: workshop report." Development 103, Supplement (1988): 25–30. http://dx.doi.org/10.1242/dev.103.supplement.25.

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We organized this workshop as an open discussion around the theme of developmental organization and evolution of the vertebrate head. To sharpen the focus of the debate initially, we, the convenors, proposed a hypothetical ‘two-step’ model of head development. The first step would be conceptually analogous to insect development, in the sense that early in embryonic development, i.e. during, or shortly after, gastrulation, a segmental pattern is specified in the neuroectoderm and/or head mesoderm. By segmentation we mean the subdivision of an embryonic field into sharply defined populations of

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Podar, Klaus, Yu-Tzu Tai, Faith E. Davies, et al. "Vascular endothelial growth factor triggers signaling cascades mediating multiple myeloma cell growth and migration." Blood 98, no. 2 (2001): 428–35. http://dx.doi.org/10.1182/blood.v98.2.428.

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Multiple myeloma (MM) remains incurable, with a median survival of 3 to 4 years. This study shows direct effects of vascular endothelial growth factor (VEGF) upon MM and plasma cell leukemia (PCL) cells. The results indicate that VEGF triggers tumor cell proliferation via a protein kinase C (PKC)–independent Raf-1–MEK–extracellular signal-regulated protein kinase pathway, and migration via a PKC-dependent pathway. These observations provide the framework for novel therapeutic strategies targeting VEGF signaling cascades in MM.

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44

Prosdocimi, Elena, Vanessa Checchetto, and Luigi Leanza. "Targeting the Mitochondrial Potassium Channel Kv1.3 to Kill Cancer Cells: Drugs, Strategies, and New Perspectives." SLAS DISCOVERY: Advancing the Science of Drug Discovery 24, no. 9 (2019): 882–92. http://dx.doi.org/10.1177/2472555219864894.

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Cancer is the consequence of aberrations in cell growth or cell death. In this scenario, mitochondria and ion channels play a critical role in regard to cell proliferation, malignant angiogenesis, migration, and metastasis. In this review, we focus on Kv1.3 and specifically on mitoKv1.3, which showed an aberrant expression in cancer cells compared with healthy tissues and which is involved in the apoptotic pathway. In recent years, mitoKv1.3 has become an oncological target since its pharmacological modulation has been demonstrated to reduce tumor growth and progression both in vitro and in vi

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Acconcia, Filippo, Christopher J. Barnes, and Rakesh Kumar. "Estrogen and Tamoxifen Induce Cytoskeletal Remodeling and Migration in Endometrial Cancer Cells." Endocrinology 147, no. 3 (2006): 1203–12. http://dx.doi.org/10.1210/en.2005-1293.

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Much research effort has been directed toward understanding how estrogen [17β-estradiol (E2)] regulates cell proliferation and motility through the rapid, direct activation of cytoplasmic signaling cascades (i.e. nongenomic signaling). Cell migration is critical to cancer cell invasion and metastasis and involves dynamic filamentous actin cytoskeletal remodeling and disassembly of focal adhesion sites. Although estrogen is recognized to induce cell migration in some model systems, very little information is available regarding the underlying pathways and potential influence of selective estrog

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Arden, Jessica D., Kari I. Lavik, Kaitlin A. Rubinic, et al. "Small-molecule agonists of mammalian Diaphanous–related (mDia) formins reveal an effective glioblastoma anti-invasion strategy." Molecular Biology of the Cell 26, no. 21 (2015): 3704–18. http://dx.doi.org/10.1091/mbc.e14-11-1502.

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The extensive invasive capacity of glioblastoma (GBM) makes it resistant to surgery, radiotherapy, and chemotherapy and thus makes it lethal. In vivo, GBM invasion is mediated by Rho GTPases through unidentified downstream effectors. Mammalian Diaphanous (mDia) family formins are Rho-directed effectors that regulate the F-actin cytoskeleton to support tumor cell motility. Historically, anti-invasion strategies focused upon mDia inhibition, whereas activation remained unexplored. The recent development of small molecules directly inhibiting or activating mDia-driven F-actin assembly that suppor

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Giese, A., R. Bjerkvig, M. E. Berens, and M. Westphal. "Cost of Migration: Invasion of Malignant Gliomas and Implications for Treatment." Journal of Clinical Oncology 21, no. 8 (2003): 1624–36. http://dx.doi.org/10.1200/jco.2003.05.063.

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Tumors of glial origin consist of a core mass and a penumbra of invasive, single cells, decreasing in numbers towards the periphery and still detectable several centimeters away from the core lesion. Several decades ago, the diffuse nature of malignant gliomas was recognized by neurosurgeons when super-radical resections using hemispherectomies failed to eradicate these tumors. Local invasiveness eventually leads to regrowth of a recurrent tumor predominantly adjacent to the resection cavity, which is not significantly altered by radiation or chemotherapy. This raises the question of whether i

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Lopez-Caraballo, Lidia, Jordi Martorell-Marugan, Pedro Carmona-Sáez, and Elena Gonzalez-Munoz. "iPS-Derived Early Oligodendrocyte Progenitor Cells from SPMS Patients Reveal Deficient In Vitro Cell Migration Stimulation." Cells 9, no. 8 (2020): 1803. http://dx.doi.org/10.3390/cells9081803.

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The most challenging aspect of secondary progressive multiple sclerosis (SPMS) is the lack of efficient regenerative response for remyelination, which is carried out by the endogenous population of adult oligoprogenitor cells (OPCs) after proper activation. OPCs must proliferate and migrate to the lesion and then differentiate into mature oligodendrocytes. To investigate the OPC cellular component in SPMS, we developed induced pluripotent stem cells (iPSCs) from SPMS-affected donors and age-matched controls (CT). We confirmed their efficient and similar OPC differentiation capacity, although w

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Hervieu, Alexia, Sara Farrah Heuss, Chi Zhang, et al. "A PI3K- and GTPase-independent Rac1-mTOR mechanism mediates MET-driven anchorage-independent cell growth but not migration." Science Signaling 13, no. 637 (2020): eaba8627. http://dx.doi.org/10.1126/scisignal.aba8627.

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Receptor tyrosine kinases (RTKs) are often overexpressed or mutated in cancers and drive tumor growth and metastasis. In the current model of RTK signaling, including that of MET, downstream phosphatidylinositol 3-kinase (PI3K) mediates both cell proliferation and cell migration, whereas the small guanosine triphosphatase (GTPase) Rac1 mediates cell migration. However, in cultured NIH3T3 and glioblastoma cells, we found that class I PI3K mediated oncogenic MET–induced cell migration but not anchorage-independent growth. In contrast, Rac1 regulated both processes in distinct ways. Downstream of

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Bonatti, Amedeo Franco, Carmelo De Maria, and Giovanni Vozzi. "Molecular Imprinting Strategies for Tissue Engineering Applications: A Review." Polymers 13, no. 4 (2021): 548. http://dx.doi.org/10.3390/polym13040548.

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Tissue Engineering (TE) represents a promising solution to fabricate engineered constructs able to restore tissue damage after implantation. In the classic TE approach, biomaterials are used alongside growth factors to create a scaffolding structure that supports cells during the construct maturation. A current challenge in TE is the creation of engineered constructs able to mimic the complex microenvironment found in the natural tissue, so as to promote and guide cell migration, proliferation, and differentiation. In this context, the introduction inside the scaffold of molecularly imprinted

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