Effects of Friction Coefficient and Receptor Number on Cell-Substrate Interactions During Migration

2010 ◽  
Author(s):  
Henry C. Wong ◽  
William C. Tang
Keyword(s):  
Cell Migration ◽  
Cancer Metastasis ◽  
Element Model ◽  
Biological Tissues ◽  
Substrate Interactions ◽  
Strain Behavior ◽  
Structural Support ◽  
Research Areas ◽  
Cell Substrate ◽  
A Cell

Biological tissues are composed of cells that adhere to the extracellular matrix (ECM) via cell-surface integrin receptors that bind to specific proteins, such as fibronectin, embedded in the matrix. In this manner, the ECM functions as a structural support for the attached cells, and mechanical forces are able to be transmitted from the cell to the ECM and vice versa [1]. Cell migration, a process that is highly dependent on these mechanical interactions, is important for many normal biological processes and diseases that occur in the human body, which include embryonic development, immune response, would healing, and cancer invasion [2]. Though many continuum models of cell migration have been proposed, there is still a need for a model that can be used to quantitatively understand the mechanical factors that can influence the movement of a cell on a substrate. This would be invaluable to the research areas of tissue engineering as well as cancer metastasis. We utilized a finite element model to elucidate the mechanism of cell-substrate interactions for a cell that consistently migrates in a single direction. Our model follows the approach taken by Gracheva and Othmer [2], but we extended their model to describe two-dimensional plane strain behavior.

Role of carbohydrates in cell-substrate interactions during newt epidermal cell migration

1987 ◽  
Vol 243 (3) ◽  
pp. 461-471 ◽  
Author(s):  
Karen Davenport Atnip ◽  
James T. Mahan ◽  
Donald J. Donaldson
Keyword(s):  
Cell Migration ◽  
Epidermal Cell ◽  
Substrate Interactions ◽  
Cell Substrate

scholarly journals Spheroids of Endothelial Cells and Vascular Smooth Muscle Cells Promote Cell Migration in Hyaluronic Acid and Fibrinogen Composite Hydrogels

Research ◽  
2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Xingang Zuo ◽  
Haolan Zhang ◽  
Tong Zhou ◽  
Yiyuan Duan ◽  
Hao Shou ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Cell Migration ◽  
Hyaluronic Acid ◽  
Cell Adhesion ◽  
Dynamic Change ◽  
Substrate Interactions ◽  
Composite Hydrogels ◽  
Cell Functions ◽  
Cell Spheroids ◽  
Cell Substrate

Cell migration plays a pivotal role in many pathological and physiological processes. So far, most of the studies have been focused on 2-dimensional cell adhesion and migration. Herein, the migration behaviors of cell spheroids in 3D hydrogels obtained by polymerization of methacrylated hyaluronic acid (HA-MA) and fibrinogen (Fg) with different ratios were studied. The Fg could be released to the medium gradually along with time prolongation, achieving the dynamic change of hydrogel structures and properties. Three types of cell spheroids, i.e., endothelial cell (EC), smooth muscle cell (SMC), and EC-SMC spheroids, were prepared with 10,000 cells in each, whose diameters were about 343, 108, and 224 μm, respectively. The composite hydrogels with an intermediate ratio of Fg allowed the fastest 3D migration of cell spheroids. The ECs-SMCs migrated longest up to 3200 μm at day 14, whereas the SMC spheroids migrated slowest with a distance of only ~400 μm at the same period of time. The addition of free RGD or anti-CD44 could significantly reduce the migration distance, revealing that the cell-substrate interactions take the major roles and the migration is mesenchymal dependent. Moreover, addition of anti-N-cadherin and MMP inhibitors also slowed down the migration rate, demonstrating that the degradation of hydrogels and cell-cell interactions are also largely involved in the cell migration. RT-PCR measurement showed that expression of genes related to cell adhesion and antiapoptosis, and angiogenesis was all upregulated in the EC-SMC spheroids than single EC or SMC spheroids, suggesting that the use of composite cell spheroids is more promising to promote cell-substrate interactions and maintenance of cell functions.

The theme trends and knowledge structure of H19 gene in cancer research: a scientometric analysis (Preprint)

2019 ◽  
Author(s):  
Zhigang Cui ◽  
Zhihua Yin ◽  
Lei Cui
Keyword(s):  
Cancer Research ◽  
Social Network ◽  
Citation Analysis ◽  
High Frequency ◽  
Cancer Metastasis ◽  
Intellectual Structure ◽  
Scientometric Analysis ◽  
Research Areas ◽  
Pivotal Study ◽  
Matrix Construction

BACKGROUND Background:H19 gene is maternally expressed imprinted oncofetal gene. This study aimed to explore distribution pattern and intellectual structure of H19 in cancer. OBJECTIVE Published scientific 826 papers related to H19 from Jan 1st, 2000 to March 22st, 2019 were obtained from the Web of Science core collection. METHODS We performed extraction of keywords and co-word matrix construction using BICOMB software. Then gCLUTO software, ucinet, excel software, Citespace, Vosviewer were successfully used for double -cluster analysis, social network analysis, Strategic coordinate analysis, co-citation analysis, and journal analysis. RESULTS We analyzed the distributions of included article of H19, identified 34 high-frequency keywords and classified them into 6 categories. Through co-word analysis and co-citation analysis for these categories, we identified the hotspot areas and intellectual basis about H19 in cancer research. Then the prospects of hotspots and their associations were accesssed by strategic coordinate diagrams and social network diagrams. CONCLUSIONS 6 research categories of 34 high-frequency keywords could represent the theme trends on H19 to some extent. Mir-675, cancer metastasis and risk, Wnt/β-catenin signaling pathway, SNP, and ceRNA network were core and mature research areas in this field. There is a lack of promising areas of H19 research. Matouk(2006) article play a key role in H19 research, and Murphy SK(2006)and Luo M(2013) articles serve knowledge transmission as pivotal study.

scholarly journals Erianthridin suppresses non-small-cell lung cancer cell metastasis through inhibition of Akt/mTOR/p70S6K signaling pathway

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Sutthaorn Pothongsrisit ◽  
Kuntarat Arunrungvichian ◽  
Yoshihiro Hayakawa ◽  
Boonchoo Sritularak ◽  
Supachoke Mangmool ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Migration ◽  
Protein Kinase ◽  
Small Cell Lung Cancer ◽  
Cancer Metastasis ◽  
Small Cell ◽  
Migration And Invasion ◽  
Lung Cancer Cell ◽  
Small Cell Lung ◽  
Cell Metastasis

AbstractCancer metastasis is a major cause of the high mortality rate in lung cancer patients. The cytoskeletal rearrangement and degradation of extracellular matrix are required to facilitate cell migration and invasion and the suppression of these behaviors is an intriguing approach to minimize cancer metastasis. Even though Erianthridin (ETD), a phenolic compound isolated from the Thai orchid Dendrobium formosum exhibits various biological activities, the molecular mechanism of ETD for anti-cancer activity is unclear. In this study, we found that noncytotoxic concentrations of ETD (≤ 50 μM) were able to significantly inhibit cell migration and invasion via disruption of actin stress fibers and lamellipodia formation. The expression of matrix metalloproteinase-2 (MMP-2) and MMP-9 was markedly downregulated in a dose-dependent manner after ETD treatment. Mechanistic studies revealed that protein kinase B (Akt) and its downstream effectors mammalian target of rapamycin (mTOR) and p70 S6 kinase (p70S6K) were strongly attenuated. An in silico study further demonstrated that ETD binds to the protein kinase domain of Akt with both hydrogen bonding and van der Waals interactions. In addition, an in vivo tail vein injection metastasis study demonstrated a significant effect of ETD on the suppression of lung cancer cell metastasis. This study provides preclinical information regarding ETD, which exhibits promising antimetastatic activity against non-small-cell lung cancer through Akt/mTOR/p70S6K-induced actin reorganization and MMPs expression.

scholarly journals Ovalitenone Inhibits the Migration of Lung Cancer Cells via the Suppression of AKT/mTOR and Epithelial-to-Mesenchymal Transition

Molecules ◽  
2021 ◽  
Vol 26 (3) ◽  
pp. 638
Author(s):  
Kittipong Sanookpan ◽  
Nongyao Nonpanya ◽  
Boonchoo Sritularak ◽  
Pithi Chanvorachote
Keyword(s):  
Lung Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Colony Formation ◽  
Cancer Metastasis ◽  
Epithelial To Mesenchymal Transition ◽  
A549 Cells ◽  
Lung Cancer Cells ◽  
Migration And Invasion ◽  
Mesenchymal Transition

Cancer metastasis is the major cause of about 90% of cancer deaths. As epithelial-to-mesenchymal transition (EMT) is known for potentiating metastasis, this study aimed to elucidate the effect of ovalitenone on the suppression of EMT and metastasis-related behaviors, including cell movement and growth under detached conditions, and cancer stem cells (CSCs), of lung cancer cells. Methods: Cell viability and cell proliferation were determined by 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazo-liumbromide (MTT) and colony formation assays. Cell migration and invasion were analyzed using a wound-healing assay and Boyden chamber assay, respectively. Anchorage-independent cell growth was determined. Cell protrusions (filopodia) were detected by phalloidin-rhodamine staining. Cancer stem cell phenotypes were assessed by spheroid formation. The proteins involved in cell migration and EMT were evaluated by Western blot analysis and immunofluorescence staining. Results: Ovalitenone was used at concentrations of 0–200 μM. While it caused no cytotoxic effects on lung cancer H460 and A549 cells, ovalitenone significantly suppressed anchorage-independent growth, CSC-like phenotypes, colony formation, and the ability of the cancer to migrate and invade cells. The anti-migration activity was confirmed by the reduction of filopodia in the cells treated with ovalitenone. Interestingly, we found that ovalitenone could significantly decrease the levels of N-cadherin, snail, and slug, while it increased E-cadherin, indicating EMT suppression. Additionally, the regulatory signaling of focal adhesion kinase (FAK), ATP-dependent tyrosine kinase (AKT), the mammalian target of rapamycin (mTOR), and cell division cycle 42 (Cdc42) was suppressed by ovalitenone. Conclusions: The results suggest that ovalitenone suppresses EMT via suppression of the AKT/mTOR signaling pathway. In addition, ovalitenone exhibited potential for the suppression of CSC phenotypes. These data reveal the anti-metastasis potential of the compound and support the development of ovalitenone treatment for lung cancer therapy.

scholarly journals Eosinophilic inflammation promotes CCL6-dependent metastatic tumor growth

2021 ◽  
Vol 7 (22) ◽  
pp. eabb5943
Author(s):  
Fei Li ◽  
Xufei Du ◽  
Fen Lan ◽  
Na Li ◽  
Chao Zhang ◽  
...  
Keyword(s):  
Cell Migration ◽  
Bone Metastasis ◽  
Tumor Cell ◽  
Cancer Metastasis ◽  
Inflammatory Diseases ◽  
Metastatic Tumor ◽  
Eosinophil Infiltration ◽  
Tumor Cell Migration ◽  
Promote Tumor Cell ◽  
Chemokine Ligand

Compelling evidence suggests that inflammatory components contribute to cancer development. However, eosinophils, involved in several inflammatory diseases, were not fully explored in cancer metastasis. We show that airway inflammatory eosinophilia and colonic inflammation with eosinophil infiltration are both associated with increased metastasis in mice. Eosinophilia is responsible for increased bone metastasis in eosinophil-enriched Cd3δ-Il-5 transgenic (Il-5 Tg) mice. We also observe increased eosinophils in the malignant pleural effusion of cancer patients with pleural metastasis. Mechanistically, eosinophils promote tumor cell migration and metastasis formation through secreting C-C motif chemokine ligand 6 (CCL6). Genetic knockout of Ccl6 in Il-5 Tg mice remarkably attenuates bone metastasis. Moreover, inhibition of C-C chemokine receptor 1 (CCR1, the receptor of CCL6) in tumor cells reduces tumor cell migration and metastasis. Thus, our study identifies a CCL6-dependent prometastatic activity of eosinophils, which can be inhibited by targeting CCR1 and represent an approach to preventing metastatic disease.

Production and Analysis of High Resolution Polymer Replicas of Fibrillar Collagen

1999 ◽  
Vol 5 (S2) ◽  
pp. 398-399
Author(s):  
P. Sims ◽  
B. Todd ◽  
S. Eppell ◽  
T. Li ◽  
K. Park ◽  
...  
Keyword(s):  
Cellular Response ◽  
Physical Nature ◽  
Cell Types ◽  
Artificial Substrates ◽  
Adherent Cell ◽  
Fibrillar Collagen ◽  
New Materials ◽  
Substrate Interactions ◽  
Number Of Factors ◽  
Cell Substrate

Adherent cells generally construct the immediate substrate upon which they reside. This may occur via synthesis and secretion of new materials and/or by rearrangement and modification of existing substrate. The response of adherent cell types to an existing substrate can be influenced by a number of factors which include both the chemical and physical nature of the substrate. Cell adhesion, proliferation, differentiation and death can all be substrate dependent. Much effort has been directed toward chemical modification of substrates to regulate one or more of the parameters noted above. A significant, but somewhat smaller, degree of attention has been paid to the effects of the topography and microtopography on the cell response to substrate materials. Studies to date strongly suggest the topography is a significant factor in cell-substrate interactions. As noted above, it is most probable that both the chemistry and the structure of a substrate simultaneously influence the cellular response. However we wished to determine, particularly for artificial substrates, the role which microtopography can play in cell-substrate interactions.

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