Journal articles: 'Cells Motility'

1

ULFENDAHL, M. "Motility in auditory sensory cells." Acta Physiologica Scandinavica 130, no. 3 (July 1987): 521–27. http://dx.doi.org/10.1111/j.1748-1716.1987.tb08171.x.

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Pate, Jack L. "Gliding motility in procaryotic cells." Canadian Journal of Microbiology 34, no. 4 (April 1, 1988): 459–65. http://dx.doi.org/10.1139/m88-079.

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Recho, Pierre, Thibaut Putelat, and Lev Truskinovsky. "Mechanics of motility initiation and motility arrest in crawling cells." Journal of the Mechanics and Physics of Solids 84 (November 2015): 469–505. http://dx.doi.org/10.1016/j.jmps.2015.08.006.

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Schwab, Albrecht, Peter Hanley, Anke Fabian, and Christian Stock. "Potassium Channels Keep Mobile Cells on the Go." Physiology 23, no. 4 (August 2008): 212–20. http://dx.doi.org/10.1152/physiol.00003.2008.

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Cell motility is a prerequisite for the creation of new life, and it is required for maintaining the integrity of an organism. Under pathological conditions, “too much” motility may cause premature death. Studies over the past few years have revealed that ion channels are essential for cell motility. This review highlights the importance of K+ channels in regulating cell motility.

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Sarna, Sushil K. "Are interstitial cells of Cajal plurifunction cells in the gut?" American Journal of Physiology-Gastrointestinal and Liver Physiology 294, no. 2 (February 2008): G372—G390. http://dx.doi.org/10.1152/ajpgi.00344.2007.

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The proposed functions of the interstitial cells of Cajal (ICC) are to 1) pace the slow waves and regulate their propagation, 2) mediate enteric neuronal signals to smooth muscle cells, and 3) act as mechanosensors. In addition, impairments of ICC have been implicated in diverse motility disorders. This review critically examines the available evidence for these roles and offers alternate explanations. This review suggests the following: 1) The ICC may not pace the slow waves or help in their propagation. Instead, they may help in maintaining the gradient of resting membrane potential (RMP) through the thickness of the circular muscle layer, which stabilizes the slow waves and enhances their propagation. The impairment of ICC destabilizes the slow waves, resulting in attenuation of their amplitude and impaired propagation. 2) The one-way communication between the enteric neuronal varicosities and the smooth muscle cells occurs by volume transmission, rather than by wired transmission via the ICC. 3) There are fundamental limitations for the ICC to act as mechanosensors. 4) The ICC impair in numerous motility disorders. However, a cause-and-effect relationship between ICC impairment and motility dysfunction is not established. The ICC impair readily and transform to other cell types in response to alterations in their microenvironment, which have limited effects on motility function. Concurrent investigations of the alterations in slow-wave characteristics, excitation-contraction and excitation-inhibition couplings in smooth muscle cells, neurotransmitter synthesis and release in enteric neurons, and the impairment of the ICC are required to understand the etiologies of clinical motility disorders.

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Coelho Neto, José, and Oscar Nassif Mesquita. "Living cell motility." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 366, no. 1864 (August 2, 2007): 319–28. http://dx.doi.org/10.1098/rsta.2007.2091.

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The motility of living eukaryotic cells is a complex process driven mainly by polymerization and depolymerization of actin filaments underneath the plasmatic membrane (actin cytoskeleton). However, the exact mechanisms through which cells are able to control and employ ‘actin-generated’ mechanical forces, in order to change shape and move in a well-organized and coordinated way, are not quite established. Here, we summarize the experimental results obtained by our research group during recent years in studying the motion of living cells, such as macrophages and erythrocytes. By using our recently developed defocusing microscopy technique, which allows quantitative analysis of membrane surface dynamics of living cells using a simple bright-field optical microscope, we were able to analyse morphological and dynamical parameters of membrane ruffles and small membrane fluctuations, study the process of phagocytosis and also measure values for cell refractive index, membrane bending modulus and cell viscosity. Although many questions still remain unanswered, our data seem to corroborate some aspects of recent physical models of cell membranes and motility.

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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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Melkonian, M. "Centrin-Mediated Motility: A Novel Cell Motility Mechanism in Eukaryotic Cells." Botanica Acta 102, no. 1 (February 1989): 3–4. http://dx.doi.org/10.1111/j.1438-8677.1989.tb00059.x.

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Xu, X., W. E. I. Li, G. Y. Huang, R. Meyer, T. Chen, Y. Luo, M. P. Thomas, G. L. Radice, and C. W. Lo. "Modulation of mouse neural crest cell motility by N-cadherin and connexin 43 gap junctions." Journal of Cell Biology 154, no. 1 (July 9, 2001): 217–30. http://dx.doi.org/10.1083/jcb.200105047.

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Connexin 43 (Cx43α1) gap junction has been shown to have an essential role in mediating functional coupling of neural crest cells and in modulating neural crest cell migration. Here, we showed that N-cadherin and wnt1 are required for efficient dye coupling but not for the expression of Cx43α1 gap junctions in neural crest cells. Cell motility was found to be altered in the N-cadherin–deficient neural crest cells, but the alterations were different from that elicited by Cx43α1 deficiency. In contrast, wnt1-deficient neural crest cells showed no discernible change in cell motility. These observations suggest that dye coupling may not be a good measure of gap junction communication relevant to motility. Alternatively, Cx43α1 may serve a novel function in motility. We observed that p120 catenin (p120ctn), an Armadillo protein known to modulate cell motility, is colocalized not only with N-cadherin but also with Cx43α1. Moreover, the subcellular distribution of p120ctn was altered with N-cadherin or Cx43α1 deficiency. Based on these findings, we propose a model in which Cx43α1 and N-cadherin may modulate neural crest cell motility by engaging in a dynamic cross-talk with the cell's locomotory apparatus through p120ctn signaling.

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Shea, C., J. W. Nunley, and H. E. Smith-Somerville. "Variable expression of gliding and swimming motility in Deleya marina." Canadian Journal of Microbiology 37, no. 11 (November 1, 1991): 808–14. http://dx.doi.org/10.1139/m91-140.

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Surface-associated motility has been observed in the Deleya marina type strain ATCC 25374 (strain 219). Slime tracks and a complex growth pattern, characteristic of gliding motility, developed on semisolid marine-agar motility plates. Cell movement observed by light microscopy consisted of rapid glides and flips by single cells and groups of cells. Following the development of the gliding cell growth pattern, a subpopulation of swimming cells appeared. The variation in motility was random and reversible in subculture. Electron microscopic comparisons of cells of the two motility types showed that gliding cells had no obvious motility organelles, whereas swimming cells had polar flagella. Variable expression of gliding and swimming motility was also observed in D. marina strain 140 (ATCC 27129) and in two other species of the Deleya genus. Key words: gliding, morphological variation, Deleya, biofouling.

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Jing, Zhixin, Zachary L. Benet, and David R. Fooksman. "Plasma cells Dynamics in the Bone Marrow Niche." Journal of Immunology 206, no. 1_Supplement (May 1, 2021): 11.02. http://dx.doi.org/10.4049/jimmunol.206.supp.11.02.

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Abstract Plasma cells (PCs) can become long-lived with age to maintain prophylactic antibody titer for decades in the bone marrow (BM) microenvironment that are enriched in supporting chemokines and pro-survival cytokines. It has been that PCs are sessile in the BM to receive various pro-survival signals, but how they access these signals in the dynamic BM microenvironment remains unknown. Here by establishing long-term intravital imaging of the mouse tibial BM, we show that PCs are overall motile within the BM parenchyma with unique intermittent and heterogenous motility over time. Their motility is reduced when they are in clusters or as they enter a cluster. PC cluster formation and motility requires the pro-survival cytokine APRIL. PCs motility also requires the chemokine receptor CXCR4 and its ligand CXCL12 that are known important for PC homing to BM. CXCR4/CXCL12 signaling-triggered integrin VLA-4 activation negatively regulates PC motility in the BM. Notably, not only do PCs migrate within the BM parenchyma, but they can also egress and recirculate under steady state condition or CXCR4 and VLA4 inhibition. PC motility, clustering, and recirculation are all increased with mouse age. Thus, PC motility and cluster formation underlie a dynamic BM survival niche, contributing to PC longevity and function.

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Panopoulos, Andreas, Michael Howell, Rati Fotedar, and Robert L. Margolis. "Glioblastoma motility occurs in the absence of actin polymer." Molecular Biology of the Cell 22, no. 13 (July 2011): 2212–20. http://dx.doi.org/10.1091/mbc.e10-10-0849.

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In fibroblasts and keratocytes, motility is actin dependent, while microtubules play a secondary role, providing directional guidance. We demonstrate here that the motility of glioblastoma cells is exceptional, in that it occurs in cells depleted of assembled actin. Cells display persistent motility in the presence of actin inhibitors at concentrations sufficient to fully disassemble actin. Such actin independent motility is characterized by the extension of cell protrusions containing abundant microtubule polymers. Strikingly, glioblastoma cells exhibit no motility in the presence of microtubule inhibitors, at concentrations that disassemble labile microtubule polymers. In accord with an unconventional mode of motility, glioblastoma cells have some unusual requirements for the Rho GTPases. While Rac1 is required for lamellipodial protrusions in fibroblasts, expression of dominant negative Rac1 does not suppress glioblastoma migration. Other GTPase mutants are largely without unique effect, except dominant positive Rac1-Q61L, and rapidly cycling Rac1-F28L, which substantially suppress glioblastoma motility. We conclude that glioblastoma cells display an unprecedented mode of intrinsic motility that can occur in the absence of actin polymer, and that appears to require polymerized microtubules.

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13

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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14

Koga, Hiroaki. "Study of the motility and contractility of cultured brain-tumor cells." Journal of Neurosurgery 62, no. 6 (June 1985): 906–11. http://dx.doi.org/10.3171/jns.1985.62.6.0906.

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✓ The motility of cultured cells and contractility of their cytoplasmic microfilament system were studied in benign compared with malignant brain-tumor cells. Motility of cultured cells was continuously monitored in a perfusion chamber by a computerized microscope system equipped with an autotracking device. The contractility of the microfilament system was defined by the increase in cell motility when the cell was perfused with an antimicrofilamentous agent, cytochalasin B. The motility and contractility of malignant cells were greater than those of benign cells. The increased contractility of malignant astrocytoma cells was associated with conspicuous morphological changes on electron microscopy. No significant change was observed in the motility, contractility, or morphology in various cells during perfusion with an antimicrotubular agent, colchicine. The significant differences in the motility and contractility of benign compared with malignant cells are believed to originate from qualitative differences of the microfilament system.

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15

Miyawaki, Hironori, Shuzo Arishige, Masaya Takumida, and Yasuo Harada. "Motility of Isolated Vestibular Hair Cells." Equilibrium Research 51, Suppl-8 (1992): 95–99. http://dx.doi.org/10.3757/jser.51.suppl-8_95.

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Tanigawa, Tohru, Hironori Miyawaki, Masaya Takumida, Katsuhiro Hirakawa, Mamoru Suzuki, Naoki Hayashi, and Koji Yajin. "Motility of Isolated Vestibular Hair Cells." Equilibrium Research 55, no. 1 (1996): 20–25. http://dx.doi.org/10.3757/jser.55.20.

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Xu, Ying, Ming-Zheng Xie, and Guo-Gang Liang. "Enteric glial cells and gastrointestinal motility." World Chinese Journal of Digestology 26, no. 26 (September 18, 2018): 1537–44. http://dx.doi.org/10.11569/wcjd.v26.i26.1537.

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Suzuki, Y., A. Mobaraki, W. Al-Jahdari, Y. Yoshida, H. Sakurai, and T. Nakano. "In Vitro, Fractionation Enhances Cells Motility." International Journal of Radiation Oncology*Biology*Physics 72, no. 1 (September 2008): S719. http://dx.doi.org/10.1016/j.ijrobp.2008.06.1588.

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19

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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20

Leonardy, Simone, Iryna Bulyha, and Lotte Søgaard-Andersen. "Reversing cells and oscillating motility proteins." Molecular BioSystems 4, no. 10 (2008): 1009. http://dx.doi.org/10.1039/b806640j.

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21

Hotta, Ryo, Dipa Natarajan, Alan J. Burns, and Nikhil Thapar. "Stem cells for GI motility disorders." Current Opinion in Pharmacology 11, no. 6 (December 2011): 617–23. http://dx.doi.org/10.1016/j.coph.2011.09.004.

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22

Chicoine, Michael R., and Daniel L. Silbergeld. "Assessment of brain tumor cell motility in vivo and in vitro." Journal of Neurosurgery 82, no. 4 (April 1995): 615–22. http://dx.doi.org/10.3171/jns.1995.82.4.0615.

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✓ Brain tumor dispersal far from bulk tumor contributes to and, in some instances, dominates disease progression. Three methods were used to characterize brain tumor cell motility in vivo and in vitro: 1) 2 weeks after implantation in rat cerebral cortex, single C6 cells labeled with a fluorescent tag had migrated to brain sites greater than 16 mm distant from bulk tumor; 2) time-lapse videomicroscopy of human brain tumor cells revealed motility of 12.5 µm/hr. Ruffling leading edges and pseudopod formation were most elaborate in more malignant cells; 3) an in vitro assay was devised to quantitatively evaluate motility from a region of high cell density to one of lower cell density. Human brain tumor cells were plated in the center of a petri dish, washed, and refed, establishing a 2-cm circular zone of cells in the dish center. Motility was determined by counting cells daily at predetermined distances from the central zone perimeter. Cells were found 1 cm from the perimeter by 24 hours and 3 cm from the perimeter by 4 days. Increasing serum concentration increased motility; however, neither fibronectin nor arrest of cells in the G0 phase by hydroxyurea altered motility. The addition of cytochalasin B to block cytoskeletal assembly prevented cell motility. Motility increased with increased malignancy. Subpopulations of cells were created by clonal amplification of cells that had migrated most rapidly to the dish periphery. Although morphologically indistinguishable when compared to the original cell line from which they were derived, these subpopulations demonstrated significantly increased 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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Raje, Manoj, and Karvita B. Ahluwalia. "Motility of leukemic lymphocytes." Proceedings, annual meeting, Electron Microscopy Society of America 48, no. 3 (August 12, 1990): 368–69. http://dx.doi.org/10.1017/s0424820100159382.

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In Acute Lymphocytic Leukemia motility of lymphocytes is associated with dissemination of malignancy and establishment of metastatic foci. Normal and leukemic lymphocytes in circulation reach solid tissues where due to in adequate perfusion some cells get trapped among tissue spaces. Although normal lymphocytes reenter into circulation leukemic lymphocytes are thought to remain entrapped owing to reduced mobility and form secondary metastasis. Cell surface, transmembrane interactions, cytoskeleton and level of cell differentiation are implicated in lymphocyte mobility. An attempt has been made to correlate ultrastructural information with quantitative data obtained by Laser Doppler Velocimetry (LDV). TEM of normal & leukemic lymphocytes revealed heterogeneity in cell populations ranging from well differentiated (Fig. 1) to poorly differentiated cells (Fig. 2). Unlike other cells, surface extensions in differentiated lymphocytes appear to originate by extrusion of large vesicles in to extra cellular space (Fig. 3). This results in persistent unevenness on lymphocyte surface which occurs due to a phenomenon different from that producing surface extensions in other cells.

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Dragoi, Ana-Maria, Arthur M. Talman, and Hervé Agaisse. "Bruton's Tyrosine Kinase Regulates Shigella flexneri Dissemination in HT-29 Intestinal Cells." Infection and Immunity 81, no. 2 (December 10, 2012): 598–607. http://dx.doi.org/10.1128/iai.00853-12.

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ABSTRACTShigella flexneriis a Gram-negative intracellular pathogen that infects the intestinal epithelium and utilizes actin-based motility to spread from cell to cell.S. flexneriactin-based motility has been characterized in various cell lines, but studies in intestinal cells are limited. Here we characterizedS. flexneriactin-based motility in HT-29 intestinal cells. In agreement with studies conducted in various cell lines, we showed thatS. flexnerirelies on neural Wiskott-Aldrich Syndrome protein (N-WASP) in HT-29 cells. We tested the potential role of various tyrosine kinases involved in N-WASP activation and uncovered a previously unappreciated role for Bruton's tyrosine kinase (Btk) in actin tail formation in intestinal cells. We showed that Btk depletion led to a decrease in N-WASP phosphorylation which affected N-WASP recruitment to the bacterial surface, decreased the number of bacteria displaying actin-based motility, and ultimately affected the efficiency of spread from cell to cell. Finally, we showed that the levels of N-WASP phosphorylation and Btk expression were increased in response to infection, which suggests thatS. flexneriinfection not only triggers the production of proinflammatory factors as previously described but also manipulates cellular processes required for dissemination in intestinal cells.

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Wei, Xueming, and Wolfgang D. Bauer. "Starvation-Induced Changes in Motility, Chemotaxis, and Flagellation of Rhizobium meliloti." Applied and Environmental Microbiology 64, no. 5 (May 1, 1998): 1708–14. http://dx.doi.org/10.1128/aem.64.5.1708-1714.1998.

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ABSTRACT The changes in motility, chemotactic responsiveness, and flagellation of Rhizobium meliloti RMB7201, L5-30, and JJ1c10 were analyzed after transfer of the bacteria to buffer with no available C, N, or phosphate. Cells of these three strains remained viable for weeks after transfer to starvation buffer (SB) but lost all motility within just 8 to 72 h after transfer to SB. The rates of motility loss differed by severalfold among the strains. Each strain showed a transient, two- to sixfold increase in chemotactic responsiveness toward glutamine within a few hours after transfer to SB, even though motility dropped substantially during the same period. Strains L5-30 and JJ1c10 also showed increased responsiveness to the nonmetabolizable chemoattractant cycloleucine. Cycloleucine partially restored the motility of starving cells when added after transfer and prevented the loss of motility when included in the SB used for initial suspension of the cells. Thus, interactions between chemoattractants and their receptors appear to affect the regulation of motility in response to starvation independently of nutrient or energy source availability. Electron microscopic observations revealed that R. meliloti cells lost flagella and flagellar integrity during starvation, but not as fast, nor to such a great extent, as the cells lost motility. Even after prolonged starvation, when none of the cells were actively motile, about one-third to one-half of the initially flagellated cells retained some flagella. Inactivation of flagellar motors therefore appears to be a rapid and important response ofR. meliloti to starvation conditions. Flagellar-motor inactivation was at least partially reversible by addition of either cycloleucine or glucose. During starvation, some cells appeared to retain normal flagellation, normal motor activity, or both for relatively long periods while other cells rapidly lost flagella, motor activity, or both, indicating that starvation-induced regulation of motility may proceed differently in various cell subpopulations.

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Nieman, Marvin T., Ryan S. Prudoff, Keith R. Johnson, and Margaret J. Wheelock. "N-Cadherin Promotes Motility in Human Breast Cancer Cells Regardless of Their E-Cadherin Expression." Journal of Cell Biology 147, no. 3 (November 1, 1999): 631–44. http://dx.doi.org/10.1083/jcb.147.3.631.

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E-cadherin is a transmembrane glycoprotein that mediates calcium-dependent, homotypic cell–cell adhesion and plays a role in maintaining the normal phenotype of epithelial cells. Decreased expression of E-cadherin has been correlated with increased invasiveness of breast cancer. In other systems, inappropriate expression of a nonepithelial cadherin, such as N-cadherin, by an epithelial cell has been shown to downregulate E-cadherin expression and to contribute to a scattered phenotype. In this study, we explored the possibility that expression of nonepithelial cadherins may be correlated with increased motility and invasion in breast cancer cells. We show that N-cadherin promotes motility and invasion; that decreased expression of E-cadherin does not necessarily correlate with motility or invasion; that N-cadherin expression correlates both with invasion and motility, and likely plays a direct role in promoting motility; that forced expression of E-cadherin in invasive, N-cadherin–positive cells does not reduce their motility or invasive capacity; that forced expression of N-cadherin in noninvasive, E-cadherin–positive cells produces an invasive cell, even though these cells continue to express high levels of E-cadherin; that N-cadherin–dependent motility may be mediated by FGF receptor signaling; and that cadherin-11 promotes epithelial cell motility in a manner similar to N-cadherin.

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Starruß, Jörn, Fernando Peruani, Vladimir Jakovljevic, Lotte Søgaard-Andersen, Andreas Deutsch, and Markus Bär. "Pattern-formation mechanisms in motility mutants of Myxococcus xanthus." Interface Focus 2, no. 6 (October 3, 2012): 774–85. http://dx.doi.org/10.1098/rsfs.2012.0034.

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Formation of spatial patterns of cells is a recurring theme in biology and often depends on regulated cell motility. Motility of the rod-shaped cells of the bacterium Myxococcus xanthus depends on two motility machineries, type IV pili (giving rise to S-motility) and the gliding motility apparatus (giving rise to A-motility). Cell motility is regulated by occasional reversals. Moving M. xanthus cells can organize into spreading colonies or spore-filled fruiting bodies, depending on their nutritional status. To ultimately understand these two pattern-formation processes and the contributions by the two motility machineries, as well as the cell reversal machinery, we analyse spatial self-organization in three M. xanthus strains: (i) a mutant that moves unidirectionally without reversing by the A-motility system only, (ii) a unidirectional mutant that is also equipped with the S-motility system, and (iii) the wild-type that, in addition to the two motility systems, occasionally reverses its direction of movement. The mutant moving by means of the A-engine illustrates that collective motion in the form of large moving clusters can arise in gliding bacteria owing to steric interactions of the rod-shaped cells, without the need of invoking any biochemical signal regulation. The two-engine strain mutant reveals that the same phenomenon emerges when both motility systems are present, and as long as cells exhibit unidirectional motion only. From the study of these two strains, we conclude that unidirectional cell motion induces the formation of large moving clusters at low and intermediate densities, while it results in vortex formation at very high densities. These findings are consistent with what is known from self-propelled rod models, which strongly suggests that the combined effect of self-propulsion and volume exclusion interactions is the pattern-formation mechanism leading to the observed phenomena. On the other hand, we learn that when cells occasionally reverse their moving direction, as observed in the wild-type, cells form small but strongly elongated clusters and self-organize into a mesh-like structure at high enough densities. These results have been obtained from a careful analysis of the cluster statistics of ensembles of cells, and analysed in the light of a coagulation Smoluchowski equation with fragmentation.

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Ashmore, Jonathan. "Cochlear Outer Hair Cell Motility." Physiological Reviews 88, no. 1 (January 2008): 173–210. http://dx.doi.org/10.1152/physrev.00044.2006.

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Normal hearing depends on sound amplification within the mammalian cochlea. The amplification, without which the auditory system is effectively deaf, can be traced to the correct functioning of a group of motile sensory hair cells, the outer hair cells of the cochlea. Acting like motor cells, outer hair cells produce forces that are driven by graded changes in membrane potential. The forces depend on the presence of a motor protein in the lateral membrane of the cells. This protein, known as prestin, is a member of a transporter superfamily SLC26. The functional and structural properties of prestin are described in this review. Whether outer hair cell motility might account for sound amplification at all frequencies is also a critical question and is reviewed here.

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L Zanella, Eraldo. "Melatonin Effect on Cryopreserved Sperm Cells of Crioulo Stallions." Open Access Journal of Veterinary Science & Research 5, no. 2 (2020): 1–8. http://dx.doi.org/10.23880/oajvsr-16000202.

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The freezing/thawing process of spermatozoa can cause cellular damage to the male gamete, decreasing the fertilization potential due to the increase in the production of reactive oxygen species (ROS). Melatonin is a potent endogenous antioxidant that protects the body against the damage caused by ROS. This study has evaluated different melatonin concentrations on the sperm viability of cryopreserved semen of Crioulo stallions. For that, three ejaculates were collected from five stallions diluted in a commercial extender followed by centrifugation and resuspension in a commercial freezing extender supplemented with 0; 1.25; 2.5. 5mM of Melatonin before the cryopreservation process. After thawing, the evaluation was performed assessing motility and flow cytometry evaluations: the plasma membrane integrity (PI), the integrity of the acrosomal membrane (FITC-PNA), mitochondrial membrane potential (JC1), and ROS generation (DCF-DA). Our results showed that sperm motility in the group without Melatonin and the 1.25mM group did not show the difference; however, the groups 2.5mM and 5mM presented a reduction in sperm motility. The 1.25 mM concentration was able to protect the plasma membrane during the cryopreservation process, in addition to showing a significant reduction in the production of ROS and increasing the percentage of sperm with integral acrosome. It can also be seen that high concentrations of Melatonin did not show beneficial effects. In conclusion, the addition of 1.25 mM of the Melatonin in Crioulo sperm cells showed to have a protective effect on the sperm cell during cryopreservation.

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Ohnishi, Takanori, Norio Arita, Toru Hayakawa, Shuichi Izumoto, Takuyu Taki, and Hiroshi Yamamoto. "Motility factor produced by malignant glioma cells: role in tumor invasion." Journal of Neurosurgery 73, no. 6 (December 1990): 881–88. http://dx.doi.org/10.3171/jns.1990.73.6.0881.

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✓ To better understand the cellular mechanism of tumor invasion, the production of a cell motility-stimulating factor by malignant glioma cells was studied in vitro. Serum-free conditioned media from cultures of rat C6 and human T98G cell lines contained a factor that stimulated the locomotion of the producer cells. This factor was termed the “glioma-derived motility factor.” The glioma-derived motility factor is a heat-labile protein with a molecular weight greater than 10 kD and has relative stability to acid. The factor showed not only chemotactic activity but also chemokinetic (stimulated random locomotion) activity in the two types of glioma cells studied. Although glioma-derived motility factors in conditioned media obtained from two different cell origins are likely to be the same, chemokinetic migration of T98G cells to their conditioned medium was much stronger than that of C6 cells to theirs. Coincubation of cells with cytochalasin B, which disrupts the assembly of cellular actin microfilaments, almost completely inhibited the cell migration stimulated by glioma-derived motility factor. Cytochalasin B also induced marked alterations in cell morphology, including cell retraction and arborization, while the drug did not affect cell attachment to culture dishes. These results indicate that glioma cells produce a motility factor which may play a role particularly when tumor cells are detached and migrate away from the original tumor mass, thus promoting tumor invasion. Also, glioma cell migration stimulated by the motility factor requires the normal organization of cytoskeletons such as actin microfilaments.

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Chen, H., N. E. Paradies, M. Fedor-Chaiken, and R. Brackenbury. "E-cadherin mediates adhesion and suppresses cell motility via distinct mechanisms." Journal of Cell Science 110, no. 3 (February 1, 1997): 345–56. http://dx.doi.org/10.1242/jcs.110.3.345.

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Expression of the calcium-dependent adhesion molecule E-cadherin suppresses the invasion of cells in vitro, but the mechanism of this effect is unknown. To investigate this mechanism, we analyzed the effects of expressing E-cadherin in mouse L-cells and rat astrocyte-like WC5 cells. Increased cellular adhesion mediated by E-cadherin reduced invasion in WC5 cells and in some L-cells, but not in others. In all cases, suppression of invasion was correlated with decreased cell movement as assessed in an in vitro wound-filling assay and a transwell motility assay. To define the relationship between adhesion mediated by E-cadherin and suppression of motility, we analyzed the effects of deleting different regions of the E-cadherin cytoplasmic domain. E-cadherin lacking the entire cytoplasmic domain did not mediate calcium-dependent adhesion and did not reduce cell motility when expressed in WC5 cells. E-cadherin lacking a portion of the catenin-binding domain did not associate with the cytoskeleton and did not promote adhesion, yet still suppressed the motility of WC5 cells. In addition, E-cadherin that retains an intact catenin-binding domain, but lacks a juxtamembrane portion of the cytoplasmic domain, mediated effective adhesion, but did not suppress motility. These results indicate E-cadherin mediates adhesion and suppresses cell motility via distinct of E-cadherin plays a key role in suppressing motility.

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Ramonaite, Rima, Robertas Petrolis, Simge Unay, Gediminas Kiudelis, Jurgita Skieceviciene, Limas Kupcinskas, Mehmet Dincer Bilgin, and Algimantas Krisciukaitis. "Mathematical morphology-based imaging of gastrointestinal cancer cell motility and 5-aminolevulinic acid-induced fluorescence." Biomedical Engineering / Biomedizinische Technik 64, no. 6 (December 18, 2019): 711–20. http://dx.doi.org/10.1515/bmt-2018-0197.

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Abstract The aim of this study was the quantitative evaluation of gastrointestinal cancer cell motility and 5-aminolevulinic acid (5-ALA)-induced fluorescence in vitro using mathematical morphology and structural analysis methods. The results of our study showed that MKN28 cells derived from the lymph node have the highest motility compared with AGS or HCT116 cells derived from primary tumors. Regions of single cells were characterized as most moving, and “tightly packed” cell colonies as nearly immobile. We determined the reduction of cell motility in late passage compared to early passage. Application of 5-ALA caused fluorescence in all investigated cells, and the fluorescence was different with regard to the cell type and application time. We observed higher fluorescence in MKN28 cells. Comprehensive image analysis did not reveal any statistically significant difference in fluorescence intensity between “tightly packed” cell regions, where nearly no motility was registered and loosely distributed cells, where the highest cell motility was registered. In conclusions, our study revealed that MKN28 cells derived from the lymph node have higher motility and 5-ALA-induced fluorescence than AGS or HCT116 derived from primary tumors. Moreover, image analysis based on a large amount of processed data is an important tool to study these tumor cell properties.

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Ouasti, Sihem, Alessandro Faroni, Paul J. Kingham, Matilde Ghibaudi, Adam J. Reid, and Nicola Tirelli. "Hyaluronic Acid (HA) Receptors and the Motility of Schwann Cell(-Like) Phenotypes." Cells 9, no. 6 (June 17, 2020): 1477. http://dx.doi.org/10.3390/cells9061477.

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The cluster of differentiation 44 (CD44) and the hyaluronan-mediated motility receptor (RHAMM), also known as CD168, are perhaps the most studied receptors for hyaluronic acid (HA); among their various functions, both are known to play a role in the motility of a number of cell types. In peripheral nerve regeneration, the stimulation of glial cell motility has potential to lead to better therapeutic outcomes, thus this study aimed to ascertain the presence of these receptors in Schwann cells (rat adult aSCs and neonatal nSCs) and to confirm their influence on motility. We included also a Schwann-like phenotype (dAD-MSCs) derived from adipose-derived mesenchymal stem cells (uAD-MSCs), as a possible basis for an autologous cell therapy. CD44 was expressed similarly in all cell types. Interestingly, uAD-MSCs were RHAMM(low), whereas both Schwann cells and dASCs turned out to be similarly RHAMM(high), and indeed antibody blockage of RHAMM effectively immobilized (in vitro scratch wound assay) all the RHAMM(high) Schwann(-like) types, but not the RHAMM(low) uAD-MSCs. Blocking CD44, on the other hand, affected considerably more uAD-MSCs than the Schwann(-like) cells, while the combined blockage of the two receptors immobilized all cells. The results therefore indicate that Schwann-like cells have a specifically RHAMM-sensitive motility, where the motility of precursor cells such as uAD-MSCs is CD44- but not RHAMM-sensitive; our data also suggest that CD44 and RHAMM may be using complementary motility-controlling circuits.

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Braun, Timothy F., Manjeet K. Khubbar, Daad A. Saffarini, and Mark J. McBride. "Flavobacterium johnsoniae Gliding Motility Genes Identified by mariner Mutagenesis." Journal of Bacteriology 187, no. 20 (October 15, 2005): 6943–52. http://dx.doi.org/10.1128/jb.187.20.6943-6952.2005.

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ABSTRACT Cells of Flavobacterium johnsoniae glide rapidly over surfaces. The mechanism of F. johnsoniae gliding motility is not known. Eight gld genes required for gliding motility have been described. Disruption of any of these genes results in complete loss of gliding motility, deficiency in chitin utilization, and resistance to bacteriophages that infect wild-type cells. Two modified mariner transposons, HimarEm1 and HimarEm2, were constructed to allow the identification of additional motility genes. HimarEm1 and HimarEm2 each transposed in F. johnsoniae, and nonmotile mutants were identified and analyzed. Four novel motility genes, gldK, gldL, gldM, and gldN, were identified. GldK is similar in sequence to the lipoprotein GldJ, which is required for gliding. GldL, GldM, and GldN are not similar in sequence to proteins of known function. Cells with mutations in gldK, gldL, gldM, and gldN were defective in motility and chitin utilization and were resistant to bacteriophages that infect wild-type cells. Introduction of gldA, gldB, gldD, gldFG, gldH, gldI, and gldJ and the region spanning gldK, gldL, gldM, and gldN individually into 50 spontaneous and chemically induced nonmotile mutants restored motility to each of them, suggesting that few additional F. johnsoniae gld genes remain to be identified.

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Hunnicutt, David W., and Mark J. McBride. "Cloning and Characterization of theFlavobacterium johnsoniae Gliding Motility GenesgldD and gldE." Journal of Bacteriology 183, no. 14 (July 15, 2001): 4167–75. http://dx.doi.org/10.1128/jb.183.14.4167-4175.2001.

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ABSTRACT Cells of Flavobacterium johnsoniae move over surfaces by a process known as gliding motility. The mechanism of this form of motility is not known. Cells of F. johnsoniaepropel latex spheres along their surfaces, which is thought to be a manifestation of the motility machinery. Three of the genes that are required for F. johnsoniae gliding motility,gldA, gldB, and ftsX, have recently been described. Tn4351 mutagenesis was used to identify another gene, gldD, that is needed for gliding. Tn4351-induced gldD mutants formed nonspreading colonies, and cells failed to glide. They also lacked the ability to propel latex spheres and were resistant to bacteriophages that infect wild-type cells. Introduction of wild-type gldD into the mutants restored motility, ability to propel latex spheres, and sensitivity to bacteriophage infection. gldD codes for a cytoplasmic membrane protein that does not exhibit strong sequence similarity to proteins of known function. gldE, which lies immediately upstream ofgldD, encodes another cytoplasmic membrane protein that may be involved in gliding motility. Overexpression ofgldE partially suppressed the motility defects of agldB point mutant, suggesting that GldB and GldE may interact. GldE exhibits sequence similarity to Borrelia burgdorferi TlyC and Salmonella enterica serovar Typhimurium CorC.

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Liu, Hsiao-Chuan, Eun Ji Gang, Hye Na Kim, Yongsheng Ruan, Heather Ogana, Zesheng Wan, Halvard Bönig, K. Kirk Shung, and Yong-Mi Kim. "Characterizing the Motility of Chemotherapeutics-Treated Acute Lymphoblastic Leukemia Cells by Time-Lapse Imaging." Cells 9, no. 6 (June 16, 2020): 1470. http://dx.doi.org/10.3390/cells9061470.

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Drug resistance is an obstacle in the therapy of acute lymphoblastic leukemia (ALL). Whether the physical properties such as the motility of the cells contribute to the survival of ALL cells after drug treatment has recently been of increasing interest, as they could potentially allow the metastasis of solid tumor cells and the migration of leukemia cells. We hypothesized that chemotherapeutic treatment may alter these physical cellular properties. To investigate the motility of chemotherapeutics-treated B-cell ALL (B-ALL) cells, patient-derived B-ALL cells were treated with chemotherapy for 7 days and left for 12 h without chemotherapeutic treatment. Two parameters of motility were studied, velocity and migration distance, using a time-lapse imaging system. The study revealed that compared to non-chemotherapeutically treated B-ALL cells, B-ALL cells that survived chemotherapy treatment after 7 days showed reduced motility. We had previously shown that Tysabri and P5G10, antibodies against the adhesion molecules integrins α4 and α6, respectively, may overcome drug resistance mediated through leukemia cell adhesion to bone marrow stromal cells. Therefore, we tested the effect of integrin α4 or α6 blockade on the motility of chemotherapeutics-treated ALL cells. Only integrin α4 blockade decreased the motility and velocity of two chemotherapeutics-treated ALL cell lines. Interestingly, integrin α6 blockade did not affect the velocity of chemoresistant ALL cells. This study explores the physical properties of the movements of chemoresistant B-ALL cells and highlights a potential link to integrins. Further studies to investigate the underlying mechanism are warranted.

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Hiraiwa, Takumi, Takahiro G. Yamada, Norihisa Miki, Akira Funahashi, and Noriko Hiroi. "Activation of cell migration via morphological changes in focal adhesions depends on shear stress in MYCN-amplified neuroblastoma cells." Journal of The Royal Society Interface 16, no. 152 (March 2019): 20180934. http://dx.doi.org/10.1098/rsif.2018.0934.

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Neuroblastoma is the most common solid tumour of childhood, and it metastasizes to distant organs. However, the mechanism of metastasis, which generally depends on the cell motility of the neuroblastoma, remains unclear. In many solid tumours, it has been reported that shear stress promotes metastasis. Here, we investigated the relationship between shear stress and cell motility in the MYCN-amplified human neuroblastoma cell line IMR32, using a microfluidic device. We confirmed that most of the cells migrated downstream, and cell motility increased dramatically when the cells were exposed to a shear stress of 0.4 Pa, equivalent to that expected in vivo . We observed that the morphological features of focal adhesion were changed under a shear stress of 0.4 Pa. We also investigated the relationship between malignancy and the motility of IMR32 cells under shear stress. Decreasing the expression of MYCN in IMR32 cells via siRNA transfection inhibited cell motility by a shear stress of 0.4 Pa. These results suggest that MYCN-amplified neuroblastoma cells under high shear stress migrate to distant organs due to high cell motility, allowing cell migration to lymphatic vessels and venules.

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Creppy, A., F. Plouraboué, O. Praud, and A. Viel. "Collective motility of sperm in confined cells." Computer Methods in Biomechanics and Biomedical Engineering 16, sup1 (July 2013): 11–12. http://dx.doi.org/10.1080/10255842.2013.815899.

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NAKAMURA, Kei-ichiro, Kiyomasa NISHII, and Yosaburo SHIBATA. "Networks of pacemaker cells for gastrointestinal motility." Folia Pharmacologica Japonica 123, no. 3 (2004): 134–40. http://dx.doi.org/10.1254/fpj.123.134.

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Small, J. V. "Microfilament-based motility in non-muscle cells." Current Opinion in Cell Biology 1, no. 1 (February 1989): 75–79. http://dx.doi.org/10.1016/s0955-0674(89)80040-7.

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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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Rieken, S., J. Rieber, S. Brons, D. Habermehl, H. Rief, L. Orschiedt, K. Lindel, K. J. Weber, J. Debus, and S. E. Combs. "Radiation-induced motility alterations in medulloblastoma cells." Journal of Radiation Research 56, no. 3 (March 2, 2015): 430–36. http://dx.doi.org/10.1093/jrr/rru120.

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Chen, Xiangyu, and Susan A. Rotenberg. "PhosphoMARCKS drives motility of mouse melanoma cells." Cellular Signalling 22, no. 7 (July 2010): 1097–103. http://dx.doi.org/10.1016/j.cellsig.2010.03.003.

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Paksa, Azadeh, and Erez Raz. "Zebrafish germ cells: motility and guided migration." Current Opinion in Cell Biology 36 (October 2015): 80–85. http://dx.doi.org/10.1016/j.ceb.2015.07.007.

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Prag, Søren, Eugene A. Lepekhin, Kateryna Kolkova, Rasmus Hartmann-Petersen, Anna Kawa, Peter S. Walmod, Vadym Belman, et al. "NCAM regulates cell motility." Journal of Cell Science 115, no. 2 (January 15, 2002): 283–92. http://dx.doi.org/10.1242/jcs.115.2.283.

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Cell migration is required during development of the nervous system. The regulatory mechanisms for this process, however, are poorly elucidated. We show here that expression of or exposure to the neural cell adhesion molecule (NCAM) strongly affected the motile behaviour of glioma cells independently of homophilic NCAM interactions. Expression of the transmembrane 140 kDa isoform of NCAM (NCAM-140) caused a significant reduction in cellular motility, probably through interference with factors regulating cellular attachment, as NCAM-140-expressing cells exhibited a decreased attachment to a fibronectin substratum compared with NCAM-negative cells. Ectopic expression of the cytoplasmic part of NCAM-140 also inhibited cell motility, presumably via the non-receptor tyrosine kinase p59fyn with which NCAM-140 interacts. Furthermore, we showed that the extracellular part of NCAM acted as a paracrine inhibitor of NCAM-negative cell locomotion through a heterophilic interaction with a cell-surface receptor. As we showed that the two N-terminal immunoglobulin modules of NCAM, which are known to bind to heparin, were responsible for this inhibition, we presume that this receptor is a heparan sulfate proteoglycan. A model for the inhibitory effect of NCAM is proposed, which involves competition between NCAM and extracellular components for the binding to membrane-associated heparan sulfate proteoglycan.

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Spormann, Alfred M., and Dale Kaiser. "Gliding Mutants of Myxococcus xanthuswith High Reversal Frequencies and Small Displacements." Journal of Bacteriology 181, no. 8 (April 15, 1999): 2593–601. http://dx.doi.org/10.1128/jb.181.8.2593-2601.1999.

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ABSTRACT Myxococcus xanthus cells move on a solid surface by gliding motility. Several genes required for gliding motility have been identified, including those of the A- and S-motility systems as well as the mgl and frz genes. However, the cellular defects in gliding movement in many of these mutants were unknown. We conducted quantitative, high-resolution single-cell motility assays and found that mutants defective inmglAB or in cglB, an A-motility gene, reversed the direction of gliding at frequencies which were more than 1 order of magnitude higher than that of wild type cells (2.9 min−1for ΔmglAB mutants and 2.7 min−1 forcglB mutants, compared to 0.17 min−1 for wild-type cells). The average gliding speed of ΔmglABmutant cells was 40% of that of wild-type cells (on average 1.9 μm/min for ΔmglAB mutants, compared to 4.4 μm/min for wild-type cells). The mglA-dependent reversals and gliding speeds were dependent on the level of intracellular MglA protein: mglB mutant cells, which contain only 15 to 20% of the wild-type level of MglA protein, glided with an average reversal frequency of about 1.8 min−1 and an average speed of 2.6 μm/min. These values range between those exhibited by wild-type cells and by ΔmglAB mutant cells. Epistasis analysis of frz mutants, which are defective in aggregation and in single-cell reversals, showed that a frzD mutation, but not a frzE mutation, partially suppressed themglA phenotype. In contrast to mgl mutants,cglB mutant cells were able to move with wild-type speeds only when in close proximity to each other. However, under those conditions, these mutant cells were found to glide less often with those speeds. By analyzing double mutants, the high reversing movements and gliding speeds of cglB cells were found to be strictly dependent on type IV pili, encoded by S-motility genes, whereas the high-reversal pattern ofmglAB cells was only partially reduced by apilR mutation. These results suggest that the MglA protein is required for both control of reversal frequency and gliding speed and that in the absence of A motility, type IV pilus-dependent cell movement includes reversals at high frequency. Furthermore, mglAB mutants behave as if they were severely defective in A motility but only partially defective in S motility.

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Rezvan, Ali, Gabrielle Romain, Mohsen Fathi, Darren Heeke, Melisa Martinez-Paniagua, Xingyue An, Irfan N. Bandey, et al. "Multiomic dynamic single-cell profiling of CAR T cell populations associated with efficacy." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 54.18. http://dx.doi.org/10.4049/jimmunol.208.supp.54.18.

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Abstract T-cell therapy with specificity redirected through chimeric antigen receptors (CARs) has shown efficacy for the treatment of hematologic malignancies. Although treatment with CAR T cell can result in high response rates, the properties of the cells that comprise the cellular infusion product, associated with clinical benefit are incompletely understood. We utilized a suite of high-throughput single-cell assays including single-cell RNA-sequencing (scRNA-seq); confocal microscopy; and Timelapse Imaging Microscopy In Nanowell Grids (TIMING). TIMING profiling of a cohort of 16 patients showed that persistent motility of T cells in the presence of tumor cells was associated with both serial killing capacity and polyfunctionality. Confocal microscopy on these same T cells revealed that persistent motility is linearly correlated with both mitochondrial volume and lysosomal number. ScRNA-seq demonstrated that T cells from responders were enriched in pathways related to T-cell proliferative capacity; interferon responses; and a distinct cluster of pathways related to actin cytoskeleton and migration. We employed a marker-free sorting strategy for enriching T cells with persistent motility. RNA-seq on sorted motile T cells showed an enrichment of the core motility signature. These motile T cells also demonstrated superior in vivo anti-leukemia efficacy in comparison to unsorted T cells. Lastly, we also confirmed the association with increased persistent motility and killing of CAR T cells across diverse CARs. In aggregate, our data identified that independent of CAR design or biomanufacturing, persistent motility serves as a selectable cell-intrinsic biomarker, desired in the bioactivity of expanded CAR+ T cells.

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Rieppi, Monica, Veronica Vergani, Carmen Gatto, Gerardo Zanetta, Paola Allavena, Giulia Taraboletti, and Raffaella Giavazzi. "Mesothelial cells induce the motility of human ovarian carcinoma cells." International Journal of Cancer 80, no. 2 (January 18, 1999): 303–7. http://dx.doi.org/10.1002/(sici)1097-0215(19990118)80:2<303::aid-ijc21>3.0.co;2-w.

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Wu, Jiahao. "The activity of the Nrf2/Keap1 pathway regulates A549 Non-small-cell Lung Cancer (NSCLC) cells motility through RhoAROCK1 pathway." Theoretical and Natural Science 44, no. 1 (July 26, 2024): 227–34. http://dx.doi.org/10.54254/2753-8818/44/20240888.

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Purpose: It is observed that Nrf2 transcription factors initiate the production of proteins that play a role in regulating tumor growth, the study aims to discover whether Nrf2 will regulate cell motility in A549 NSCLC cells. The ROCK-RhoA pathway is a significant contributor to cell growth and migration, which can relate to cell motility. There might be a connection between Nrf2 and ROCK-RhoA pathway, the study aims to see whether Nrf2 regulates A549 NSCLC cell motility through ROCK-RhoA pathway. Method: The study will use wound healing assay to visualize cell motility, comparison is made between positive control group(A549 cells treated with brusatol) and negative control group(A549 cells not treated with brusatol), respectively representing the expression level of Nrf2 where it is inhibited or normal. The pathway by which Nrf2 regulates cell motility is studied by western blotting and chemiluminescence. Possible result: There are four main possible results: (1), Nrf2 regulates cell motility in A549 NSCLC cells, the pathway involved in this regulation is ROCK-RhoA pathway. (2), Nrf2 regulates cell motility in A549 cells, however, the pathway involved in this regulation requires further studies to decide. (3), There is no obvious correlation between Nrf2 expression level and cell motility, the inhibition of Nrf2 results in change of expression level of the ROCK-RhoA pathway, however. (4), There is no obvious correlation between Nrf2 expression level and cell motility, ROCK-RhoA pathway is not significantly affected by inhibition of Nrf2 expression, further studies are needed to decide pathways involved. Conclusion: The result of this study provides valuable insights for studying the role of Nrf2 in regulating cell motility and the pathway in the process. It would improve understanding of Nrf2 transcription factor, and how it interacts with pathways to carry out regulation of cell motility. The study also provides future possibilities in terms of cancer treatment and development of gene-based medicine.

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Journal articles on the topic 'Cells Motility'

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