Relevant bibliographies by topics / Cancer cells – Motility

Academic literature on the topic 'Cancer cells – Motility'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Cancer cells – Motility"

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De la Fuente, Ildefonso M., and José I. López. "Cell Motility and Cancer." Cancers 12, no. 8 (August 5, 2020): 2177. http://dx.doi.org/10.3390/cancers12082177.

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Cell migration is an essential systemic behavior, tightly regulated, of all living cells endowed with directional motility that is involved in the major developmental stages of all complex organisms such as morphogenesis, embryogenesis, organogenesis, adult tissue remodeling, wound healing, immunological cell activities, angiogenesis, tissue repair, cell differentiation, tissue regeneration as well as in a myriad of pathological conditions. However, how cells efficiently regulate their locomotion movements is still unclear. Since migration is also a crucial issue in cancer development, the goal of this narrative is to show the connection between basic findings in cell locomotion of unicellular eukaryotic organisms and the regulatory mechanisms of cell migration necessary for tumor invasion and metastases. More specifically, the review focuses on three main issues, (i) the regulation of the locomotion system in unicellular eukaryotic organisms and human cells, (ii) how the nucleus does not significantly affect the migratory trajectories of cells in two-dimension (2D) surfaces and (iii) the conditioned behavior detected in single cells as a primitive form of learning and adaptation to different contexts during cell migration. New findings in the control of cell motility both in unicellular organisms and mammalian cells open up a new framework in the understanding of the complex processes involved in systemic cellular locomotion and adaptation of a wide spectrum of diseases with high impact in the society such as cancer.
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Mandel, Savannah. "Collective motility of cancer cells in hyperthermia." Scilight 2020, no. 5 (January 31, 2020): 051106. http://dx.doi.org/10.1063/10.0000459.

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Jo, Jung, Soo Park, Semi Park, Hee Lee, Chanyang Kim, Dawoon Jung, and Si Song. "Novel Gastric Cancer Stem Cell-Related Marker LINGO2 Is Associated with Cancer Cell Phenotype and Patient Outcome." International Journal of Molecular Sciences 20, no. 3 (January 28, 2019): 555. http://dx.doi.org/10.3390/ijms20030555.

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The expression of leucine-rich repeat and immunoglobulin-like domain-containing nogo receptor-interacting protein 2 (LINGO2) has been reported in Parkinson’s disease; however, its role in other diseases is unknown. Gastric cancer is the second leading cause of cancer death. Cancer stem cells (CSC) are a subpopulation of cancer cells that contribute to the initiation and invasion of cancer. We identified LINGO2 as a CSC-associated protein in gastric cancers both in vitro and in patient-derived tissues. We studied the effect of LINGO2 on cell motility, stemness, tumorigenicity, and angiogenic capacity using cells sorted based on LINGO2 expression and LINGO2-silenced cells. Tissue microarray analysis showed that LINGO2 expression was significantly elevated in advanced gastric cancers. The overall survival of patients expressing high LINGO2 was significantly shorter than that of patients with low LINGO2. Cells expressing high LINGO2 showed elevated cell motility, angiogenic capacity, and tumorigenicity, while LINGO2 silencing reversed these properties. Silencing LINGO2 reduced kinase B (AKT)/extracellular signal-regulated kinase (ERK)/ERK kinase (MEK) phosphorylation and decreased epithelial-mesenchymal transition (EMT)-associated markers—N-Cadherin and Vimentin and stemness-associated markers— POU class 5 homeobox 1 (OCT4) and Indian hedgehog (IHH), and markedly decreased the CD44+ population. These indicate the involvement of LINGO2 in gastric cancer initiation and progression by altering cell motility, stemness, and tumorigenicity, suggesting LINGO2 as a putative target for gastric cancer treatment.
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Kariya, Yoshinobu, Midori Oyama, Yukiko Kariya, and Yasuhiro Hashimoto. "Phosphorylated Osteopontin Secreted from Cancer Cells Induces Cancer Cell Motility." Biomolecules 11, no. 9 (September 7, 2021): 1323. http://dx.doi.org/10.3390/biom11091323.

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Osteopontin (OPN) plays a pivotal role in cancer cell invasion and metastasis. Although OPN has a large number of phosphorylation sites, the functional significance of OPN phosphorylation in cancer cell motility remains unclear. In this study, we attempted to investigate whether phosphorylated OPN secreted from cancer cells affect cancer cell migration. Quantitative PCR and Western blot analyses revealed that MDA-MB435S, A549, and H460 cells highly expressed OPN, whereas the OPN expression levels in H358, MIAPaca-2, and Panc-1 cells were quite low or were not detected. Compared with the cancer cell lines with a low OPN expression, the high OPN-expressing cancer cell lines displayed a higher cell migration, and the cell migration was suppressed by the anti-OPN antibody. This was confirmed by the OPN overexpression in H358 cancer cells with a low endogenous OPN. Phos-tag ELISA showed that phosphorylated OPN was abundant in the cell culture media of A549 and H460 cells, but not in those of MDA-MB435S cells. Moreover, the A549 and H460 cell culture media, as well as the MDA-MB435S cell culture media with a kinase treatment increased cancer cell motility, both of which were abrogated by phosphatase treatment or anti-OPN antibodies. These results suggest that phosphorylated OPN secreted from cancer cells regulates cancer cell 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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Sehgal, Pravinkumar B., and Igor Tamm. "Interleukin-6 Enhances Motility of Breast Cancer Cells." Cancer Investigation 8, no. 6 (January 1990): 661–63. http://dx.doi.org/10.3109/07357909009018940.

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Thiery, JeanPaul. "Adhesion and motility of embryonic and cancer cells." Cell Differentiation and Development 27 (August 1989): 54. http://dx.doi.org/10.1016/0922-3371(89)90193-7.

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Sharma, Pooja, Van K. Lam, Christopher B. Raub, and Byung Min Chung. "Tracking Single Cells Motility on Different Substrates." Methods and Protocols 3, no. 3 (August 4, 2020): 56. http://dx.doi.org/10.3390/mps3030056.

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Motility is a key property of a cell, required for several physiological processes, including embryonic development, axon guidance, tissue regeneration, gastrulation, immune response, and cancer metastasis. Therefore, the ability to examine cell motility, especially at a single cell level, is important for understanding various biological processes. Several different assays are currently available to examine cell motility. However, studying cell motility at a single cell level can be costly and/or challenging. Here, we describe a method of tracking random cell motility on different substrates such as glass, tissue-culture polystyrene, and type I collagen hydrogels, which can be modified to generate different collagen network microstructures. In this study we tracked MDA-MB-231 breast cancer cells using The CytoSMARTTM System (Lonza Group, Basel, Switzerland) for live cell imaging and assessed the average cell migration speed using ImageJ and wrMTrck plugin. Our cost-effective and easy-to-use method allows studying cell motility at a single cell level on different substrates with varying degrees of stiffness and varied compositions. This procedure can be successfully performed in a highly accessible manner with a simple setup.
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Yilmaz, Mahmut, and Gerhard Christofori. "Mechanisms of Motility in Metastasizing Cells." Molecular Cancer Research 8, no. 5 (May 2010): 629–42. http://dx.doi.org/10.1158/1541-7786.mcr-10-0139.

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Jeoung, Nam Ho, Ae Lim Jo, and Hee Sung Park. "The effect of autocrine motility factor alone and in combination with methyl jasmonate on liver cancer cell growth." Bioscience, Biotechnology, and Biochemistry 85, no. 7 (May 14, 2021): 1711–15. http://dx.doi.org/10.1093/bbb/zbab087.

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ABSTRACT Neoplastic cells secrete autocrine motility factor (AMF) to stimulate the motility of cancer cells. In this study, AMF secreted from HT-29 colorectal cancer cells selectively suppressed liver cancer cells by downregulating pAKT and β-catenin. In addition, HT-29 AMF significantly augmented the activity of methyl jasmonate against liver cancer cells and is a promising alternative for liver cancer therapy.
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Dissertations / Theses on the topic "Cancer cells – Motility"

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Choi, Mi-Yon. "P53 mediated cell motility in H1299 lung cancer cells." VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/109.

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Studies have shown that gain-of- function mutant p53, AKT, and NFκB promote invasion and metastasis in tumor cells. Signals transduced by AKT and p53 are integrated via negative feedback between the two pathways. Tumor derived p53 was also indicated to induce NFκB gene expression. Due to the close relationship between p53/AKT and p53/NFκB, we hypothesized that AKT and NFκB can enhance motility in cells expressing mutant p53. Effects on cell motility were determined by scratch assays. CXCL5- chemokine is also known to induce cell motility. We hypothesized that enhanced cell motility by AKT and NFκB is mediated, in part, by CXCL5. CXCL5 expression levels in the presence and absence of inhibitors were determined by qRT-PCR. We also hypothesized that gain-of-function mutant p53 contributes to the activation of AKT. The effect of mutant p53 on AKT phosphorylation was investigated with a Ponasterone A- inducible mutant cell line (H1299/R175H) and vector control. These results indicated that AKT and NFκB enhance motility in cells expressing mutant p53 and this enhanced motility is, in part, mediated by CXCL5. However, AKT phosphorylation was independent of mutant p53.
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Garg, Ayush A. "Electromagnetic Fields Alter the Motility of Metastatic Breast Cancer Cells." The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1563816767104018.

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Adla, Shalini. "Characterization of the neural cell recognition molecule L1 in breast cancer cells and its role in breast cancer cell motility." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 125 p, 2008. http://proquest.umi.com/pqdweb?did=1459905751&sid=5&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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Seller, Zerrin. "Role of #alpha#4#beta#1-mediated signalling in malignant melanoma adhesion and motility." Thesis, King's College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266520.

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Tian, Jing. "Inhibition of melanoma cell motility by the snake venom disintegrin eristostatin." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 61 p, 2007. http://proquest.umi.com/pqdweb?did=1397900451&sid=10&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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Ahmad, Omaima Farid. "The Role of Filamin A in Cell Motility, Adhesion and Invasion in Ovarian Cancer Cells." University of Toledo Honors Theses / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=uthonors1503407822068426.

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Wright, Adele Hart. "The role of integrins in the differential upregulation of tumor cell motility by endothelial extracellular matrix proteins." Diss., Georgia Institute of Technology, 1999. http://hdl.handle.net/1853/17352.

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Hoppe, Andreas. "Adaptive spline method for the assessment of cell motility and its application to lesions." Thesis, University of South Wales, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341937.

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Di, Kaijun, and 狄凱軍. "The role of Id-1 on the proliferation, motility and mitotic regulationof prostate epithelial cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B38944704.

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Patel, Sabina. "The Development of Tetracycline Dependent Pancreatic Cancer Cells and the Evaluation of CapG and Gelsolin Expression on Pancreatic Cancer Cell Motility In Vitro." Thesis, University of Liverpool, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.491370.

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Precise control of the level of protein expression in cells can facilitate functional studies providing information on the role of given proteins. In this thesis, I describe the generation of tetracycline-inducible pancreatic cancer cells and the subsequent use of these in the functional characterisation of an actin capping protein, CapG. Such cells were obtained in three pancreatic cancer cell lines, Panc-I, Suit-2 and MiaPaCa-2 cells through consecutive transfections with two plasmid constructs. The first of these harboured a second-generation reverse tetracycline-controlled transactivator protein (rtTA) whilst the second, contained the gene of interest (CapG or luciferase) under the control of a tetracycline response promoter element (pTRE). Suit-2 derived tetracycline inducible clones, along with stable doxycycline-inducible hepatoma cell lines, were used to study the effect of modulating CapG expression on cell motility. Here I report that stable introduction of a pTRE2hygCapG construct into two doxycycline-inducible clones derived from Suit-2 cells, Suit-2 ptet1I and Suit-2 ptet29 clones resulted in a dose and time-dependent increase of CapG expression in response to doxycycline. Moreover, doxycycline-mediated upregulation of CapG expression led to a significant increase in the wound healing capacity of Suit-2 ptet29 cells. The expression of a related actin binding and cell motility protein, gelsolin was also determined. Immunostaining of benign (n=24 patients) and malignant (n=68 patients) pancreatic ductal cells revealed higher gelsolin expression in the malignant state (P
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Books on the topic "Cancer cells – Motility"

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Paiwand, Frouz Frozan. RHAMM, CD44 expression and erk activation are linked in malignant human breast cancer cells and are associated with cell motility. Ottawa: National Library of Canada, 1999.

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Heino, Jyrki, and Veli-Matti Ka ha ri. Cell invasion. Georgetown, Tex: Landes Bioscience, 2002.

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Wells, Alan, ed. Cell Motility in Cancer Invasion and Metastasis. Berlin/Heidelberg: Springer-Verlag, 2006. http://dx.doi.org/10.1007/b103440.

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1948-, Goldberg I. D., Rosen E. M, Long Island Jewish Medical Center., National Cancer Institute (U.S.). Laboratory of Pathology., and International Conference on Cytokines and Cell Motility (1990 : New York, N.Y.), eds. Cell motility factors. Basel: Birkhäuser Verlag, 1991.

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Wells, Alan. Cell Motility in Cancer Invasion and Metastasis. Springer, 2010.

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Wells, Alan. Cell Motility in Cancer Invasion and Metastasis (Cancer Metastasis - Biology and Treatment). Springer, 2006.

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Heino, Jyrki, and Veli-matti Kahari. Cell Invasion (Medical Intelligence Unit). Landes Bioscience, 2002.

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Cheng, C. Y. The Molecular Mechanisms in Spermatogenesis. Landes Bioscience, 2007.

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Book chapters on the topic "Cancer cells – Motility"

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Raz, A., S. Silletti, J. Timar, and K. V. Honn. "Effect of 12-HETE on the Expression of Autocrine Motility Factor-Receptor and Motility in Melanoma Cells." In Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation and Radiation Injury, 645–49. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3520-1_126.

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Partin, Alan W., James L. Mohler, and Donald S. Coffey. "Cell motility as an index of metastatic ability in prostate cancers: Results with an animal model and with human cancer cells." In Therapy for Genitourinary Cancer, 121–30. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3502-7_11.

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Hart, Ian R. "Cell adhesion, motility and cancer." In Molecular Biology for Oncologists, 103–11. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-3111-5_10.

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Kantor, Jason D., and Bruce R. Zetter. "Cell motility in breast cancer." In Mammary Tumor Cell Cycle, Differentiation, and Metastasis, 303–23. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1259-8_15.

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Bracke, Marc E., Daan De Maeseneer, Veerle Van Marck, Lara Derycke, Barbara Vanhoecke, Olivier De Wever, and Herman T. Depypere. "Cell motility and breast cancer metastasis." In Metastasis of Breast Cancer, 47–75. Dordrecht: Springer Netherlands, 2007. http://dx.doi.org/10.1007/978-1-4020-5867-7_4.

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Wu, Guang-Jer. "Enforced Expression of METCAM/MUC18 Decreases In Vitro Motility and Invasiveness and Tumorigenesis and In Vivo Tumorigenesis of Human Ovarian Cancer BG-1 Cells." In Advances in Experimental Medicine and Biology, 125–37. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-73359-9_8.

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Pienta, Kenneth J., Alan W. Partin, and Donald S. Coffey. "Cell Motility and Structural Harmonics in Prostate Cancer." In Molecular and Cellular Biology of Prostate Cancer, 65–72. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3704-5_5.

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Varani, James. "Control of cell motility during tissue invasion." In Selected Aspects of Cancer Progression: Metastasis, Apoptosis and Immune Response, 11–19. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6729-7_2.

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Brady, Donita C., Jamie K. Alan, and Adrienne D. Cox. "Rho GTPases in Regulation of Cancer Cell Motility, Invasion, and Microenvironment." In Cancer Genome and Tumor Microenvironment, 67–91. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0711-0_4.

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Tritthart, H. A., R. Hofmann-Wellenhof, J. Smolle, C. Helige, T. DeVaney, G. Gottlieb, M. Hartbauer, and H. Kerl. "Estimation of cancer cell motility (stationary and translocative) by computer-assisted image analysis." In Ersatz- und Ergänzungsmethoden zu Tierversuchen, 291–92. Vienna: Springer Vienna, 1998. http://dx.doi.org/10.1007/978-3-7091-7500-2_72.

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Conference papers on the topic "Cancer cells – Motility"

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Zielinski, Rachel, Cosmin Mihai, and Samir Ghadiali. "Multi-Scale Modeling of Cancer Cell Migration and Adhesion During Epithelial-to-Mesenchymal Transition." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53511.

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Cancer is a leading cause of death in the US, and tumor cell metastasis and secondary tumor formation are key factors in the malignancy and prognosis of the disease. The regulation of cell motility plays an important role in the migration and invasion of cancer cells into surrounding tissues. The primary modes of increased motility in cancerous tissues may include collective migration of a group of epithelial cells during tumor growth and single cell migration of mesenchymal cells after detachment from the primary tumor site [1]. In epithelial cancers, metastasizing cells lose their cell-cell adhesions, detach from the tumor mass, begin expressing mesenchymal markers, and become highly motile and invasive, a process known as epithelial-to-mesenchymal transition (EMT) (Fig. 1) [2]. Although the cellular and biochemical signaling mechanisms underlying EMT have been studied extensively, there is limited information about the biomechanical mechanisms of EMT. In particular, it is not known how changes in cell mechanics (cell stiffness, cell-cell adhesion strength, traction forces) influence the detachment, migration and invasion processes that occur during metastasis.
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Yu-Chiu Kao, Chau-Hwang Lee, and Po-Ling Kuo. "Increased hydrostatic pressure enhances motility of lung cancer cells." In 2014 36th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2014. http://dx.doi.org/10.1109/embc.2014.6944236.

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Nikkhah, Mehdi, Jeannine S. Strobl, Bhanu Peddi, Adedamola Omotosho, and Masoud Agah. "Micropattern Effect on Breast Cancer Cells Behavior on Isotropically Etched Silicon Microenvironments." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13030.

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In this paper we are investigating three dimensional (3-D) silicon-based microenvironments as potential platforms for breast cancer diagnostics. We have developed isotropically etched microstructures with a wide range of geometrical patterns for this purpose. Our results indicate that with the etched surface ratio of ∼65%, it is possible to capture 80–90% of the cancer cells within each silicon chip. After treatment of the cells with mitomycin C (to block the cell growth) more number of the cells are trapped inside the etched features for longer cultures times (72 h) suggesting that there is a directed motility and attraction of the cells toward the etched cavities and by optimally designing the etched features, the proposed platforms can be potentially used for diagnostics purposes.
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Popescu, Gabriel, Kamran Badizadegan, Ramachandra R. Dasari, and Michael S. Feld. "Motility of Live Cancer Cells Quantified by Fourier Phase Microscopy." In European Conference on Biomedical Optics. Washington, D.C.: OSA, 2005. http://dx.doi.org/10.1364/ecbo.2005.md4.

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Popescu, Gabriel, Kamran Badizadegan, Ramachandra R. Dasari, and Michael S. Feld. "Motility of live cancer cells quantified by Fourier phase microscopy." In European Conference on Biomedical Optics 2005, edited by Christian D. Depeursinge. SPIE, 2005. http://dx.doi.org/10.1117/12.632915.

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Burks, Hope E., Lyndsay Rhodes, Elizabeth Martin, Theresa Phamduy, Steven Elliot, Van Hoang, Henry Segar, et al. "Abstract 1034: ZEB2 promotes cell motility and metastasis in ER+ breast cancer cells." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1034.

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Chasiotis, I., D. C. Street, H. L. Fillmore, and G. T. Gillies. "AFM Studies of Tumor Cell Invasion." In ASME 2003 International Mechanical Engineering Congress and Exposition. ASMEDC, 2003. http://dx.doi.org/10.1115/imece2003-43293.

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Our recent investigations on human brain tumor (glioma) cell micro and nanodynamics via AFM methodologies have shown that brain tumor invadopodia (malignant cytostructural cell extensions with sensory, motility, and invasive characteristics extended by tumor cells into their environment) can assume specific geometries based on cell plating density and the location/distance of neighboring cells indicating strong cell sensing and signaling mechanisms between malignant cells and their surroundings. In certain occasions, cancer cell processes (extensions) have been found to be highly directional measuring more than 80 μm while invading neighboring cells by following a connecting straight path. Moreover, strong chemical gradients are suggested to influence the growth and motility of cell processes allowing for gradual adjustments of the direction of the invasive tumor extension. In response to external signals, tumor cell invadopodia develop micron-sized side-ligaments that follow the chemical gradients in their neighborhood and assist the reorientation of their main intrusive elements.
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Liu, Xiangfan, Huapeng Li, Mihir Rajurkar, Jennifer Cotton, Arthur Mercurio, Roger Davis, and Junhao Mao. "Abstract B07: Tead and AP1 coordinate transcription and motility in cancer cells." In Abstracts: AACR Special Conference on Developmental Biology and Cancer; November 30 - December 3, 2015; Boston, Massachusetts. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.devbiolca15-b07.

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Kiso, Marina, Fumiaki Sato, Sunao Tanaka, and Masakazu Toi. "Abstract 683: VEGFA/NRP1 signal contributes to cell adhesion and motility in breast cancer cells." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-683.

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Yang, Wan-Yu, Chih-Hsin Tang, and Jing-Yuan Chuang. "Abstract 1392: CTGF inhibits cell motility in oral cancer cells through reducing COX-2 expression." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1392.

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Reports on the topic "Cancer cells – Motility"

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Wang, Fang. Inhibition of Invasiveness and Motility of Human Breast Cancer Cells by Sphingosine-1-Phosphate. Fort Belvoir, VA: Defense Technical Information Center, August 1999. http://dx.doi.org/10.21236/ada382431.

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Wang, Fang. Inhibition of Invasiveness and Motility of Human Breast Cancer Cells by Sphingosine-1-Phosphate. Fort Belvoir, VA: Defense Technical Information Center, August 1998. http://dx.doi.org/10.21236/ada359261.

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Stoyanova, Tihomira, Veselina Uzunova, Albena Momchilova, Rumiana Tzoneva, and Iva Ugrinova. The Treatment of Breast Cancer Cells with Erufosine Leads to Actin Cytoskeleton Reorganization, Inhibition of Cell Motility, Cell Cycle Arrest and Apoptosis. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, January 2021. http://dx.doi.org/10.7546/crabs.2021.01.11.

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Ngan, Elaine, and Betty Diamond. LPP is Required for TGF-Beta Induced Motility and Invasion of Neu/ErbB-2 Expressing Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada568114.

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Kim, Edward J., and David Helfman. Characterization of Molecular Factors Critical to the S100A4 (A Metastasis-Associated Protein) - Dependent Increase in Motility of Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2004. http://dx.doi.org/10.21236/ada424207.

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Whitehead, Ian P. Regulation of Breast Cancer Cell Motility by Golgi-Mediated Signaling. Fort Belvoir, VA: Defense Technical Information Center, September 2011. http://dx.doi.org/10.21236/ada553967.

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Warren, Mary A. The Role of Plakoglobin in Breast Cancer Cell Motility and Invasion. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada408727.

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Wang, Bingcheng. EphA2 Kinase Agonists as Novel Suppressors of Both Prostate Cancer Cell Motility and Growth Structure. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada410229.

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Wang, Bingcheng. EphA2 Kinase Agonists as Novel Suppressors of Both Prostate Cancer Cell Motility and Growth: Structure-Function Relations and the Role of RAS/MPK Pathway. Fort Belvoir, VA: Defense Technical Information Center, September 2003. http://dx.doi.org/10.21236/ada422402.

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