scholarly journals Numerical Simulation of a Multiscale Cell Motility Model Based on the Kinetic Theory of Active Particles

Symmetry ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1003 ◽  
Author(s):  
Damián A. Knopoff ◽  
Juanjo Nieto ◽  
Luis Urrutia
Keyword(s):  
Extracellular Matrix ◽  
Cell Invasion ◽  
Numerical Experiments ◽  
Scaling Limit ◽  
Cell Movement ◽  
Tumor Cell Invasion ◽  
Macroscopic Model ◽  
Biological Processes ◽  
Microscopic Scale ◽  
Active Particles

In this work, we deal with a kinetic model of cell movement that takes into consideration the structure of the extracellular matrix, considering cell membrane reactions, haptotaxis, and chemotaxis, which plays a key role in a number of biological processes such as wound healing and tumor cell invasion. The modeling is performed at a microscopic scale, and then, a scaling limit is performed to derive the macroscopic model. We run some selected numerical experiments aimed at understanding cell movement and adhesion under certain documented situations, and we measure the alignment of the cells and compare it with the pathways determined by the extracellular matrix by introducing new alignment operators.

scholarly journals Role of aminopeptidase N (CD13) in tumor-cell invasion and extracellular matrix degradation

1993 ◽  
Vol 54 (1) ◽  
pp. 137-143 ◽  
Author(s):  
Ikuo Saiki ◽  
Junya Yoneda ◽  
Ichiro Azuma ◽  
Hideji Fujii ◽  
Fuminori Abe ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Tumor Cell ◽  
Cell Invasion ◽  
Aminopeptidase N ◽  
Tumor Cell Invasion ◽  
Matrix Degradation ◽  
Extracellular Matrix Degradation

scholarly journals P11.65 Insights into the mechanisms of primary brain tumor invasion

2019 ◽  
Vol 21 (Supplement_3) ◽  
pp. iii58-iii59
Author(s):  
A Bikfalvi ◽  
T Daubon ◽  
C Billottet
Keyword(s):  
Extracellular Matrix ◽  
Tumor Cell ◽  
Tumor Cells ◽  
Conformational Changes ◽  
Cell Invasion ◽  
Immune Cell ◽  
Tumor Cell Invasion ◽  
Migration And Invasion ◽  
Matricellular Proteins

Abstract We have made progress in unravelling the mechanisms of tumor cell invasion by focusing the attention on two molecular pathways including chemokines and extracellular matrix molecules. Chemokines are important mediators of cell signaling that operate both on normal cells and tumor cells and in the immune-cell compartment (Billottet et al, 2013). Among the chemokine receptors, CXCR3 mediate diverse biological functions and comes in two major isoforms the A and B isoform. We found that ligand affinities and conformational changes are very different for the A and B form. We have recently elucidated the role and mechanism of CXCR3A in GBM invasion (Boyé et al, 2017b). We demonstrated that agonist stimulation enhances in vitro cell migration and invasion in GBM cells. A major finding was that CXCR3A forms a complex with the trafficking receptor Lipoprotein-related receptor-1 (LRP1). Silencing of LRP1 leads to an increase in the magnitude of ligand-induced conformational change with CXCR3-A focalized at the cell membrane, leading to sustained receptor activity and increase in the migration. This was also clinically validated. Our study defines LRP1 as a new regulator of CXCR3 and indicates that targeting CXCR3-A in GBM may constitute a promising strategy to halt tumor cell invasion. The extracellular matrix (ECM) has morphogenic roles in tumors. Important ECM components are the matricellular proteins, called thrombospondins(THBS1-5) (Adams and Lawler 2011). We recently elucidated the complex role of THSB1 in GBM invasion (Daubon et al.2019). Global expression analysis revealed that THBS1 is up-regulated in GBMs and associated with a poor prognosis. We, furthermore, demonstrated that THBS1 did not activate TGFβ in GBM but that TGFβ1 induced the expression of THBS1 via SMAD3. Furthermore, GBM invasion is compromised when THBS1 is silenced in tumor cells. Thus, our data clearly show that THBS1 is not only involved in the regulation of angiogenesis in GBM, but also impacts the invasive behaviour of glioma cells by interacting with a molecule called CD47 expressed on the surface of GBM cells. RNA-sequencing after microdissection of central and peripheral tumour areas in a human PDX model demonstrated that THBS1 was the gene with the highest connectivity in the peripheral invasive tumour areas. Taken together, these data indicate that THBS1 plays important role in the infiltrative process in GBM. REFERENCES: Adams JC, Lawler J. Cold Spring Harb Perspect Biol. 2011;3:a009712 Billottet C, Quemener C, Bikfalvi A. Biochim Biophys Acta. 2013;1836:287- Boyé K et al. Sci Rep. 2017;7:10703 Boyé K et al. Nat Commun. 2017;8:1571 Daubon T et al, Nature Communications. Nat Commun. 2019 Mar 8;10(1):1146 Murphy-Ullrich JE, Poczatek M. Cytokine Growth Factor Rev. 2000 11:59

Tumor Cell Invasion Can Be Blocked by Modulators of Collagen Fibril Alignment That Control Assembly of the Extracellular Matrix

2016 ◽  
Vol 76 (14) ◽  
pp. 4249-4258 ◽  
Author(s):  
Moran Grossman ◽  
Nir Ben-Chetrit ◽  
Alina Zhuravlev ◽  
Ran Afik ◽  
Elad Bassat ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Tumor Cell ◽  
Cell Invasion ◽  
Collagen Fibril ◽  
Tumor Cell Invasion ◽  
Control Assembly

scholarly journals Tumor-associated Collagen Signatures: An Insight

2017 ◽  
Vol 8 (3) ◽  
pp. 224-230 ◽  
Author(s):  
V Pavithra
Keyword(s):  
Extracellular Matrix ◽  
Cell Invasion ◽  
Collagen Fiber ◽  
Diagnostic Marker ◽  
Malignant Tumors ◽  
Second Harmonic ◽  
Tumor Cell Invasion ◽  
Main Component ◽  
Second Harmonic Generation Imaging ◽  
Early Diagnostic

ABSTRACT Tumor microenvironment has a diverse capability to induce both beneficial and adverse consequences for tumorigenesis. It is a multifactorial process induced by the imbalance in the tumor cells and extracellular matrix (ECM). Collagen, the main component of ECM, is traditionally regarded as a passive barrier to resist tumor cell invasion. In recent years, collagen is marked to have its pivotal role to initiate and promote tumor progression. Remodeling of collagen has been appreciated in various benign and malignant tumors. These alterations can be identified and demonstrated as tumor-associated collagen signatures that can be demonstrated using second harmonic generation imaging. Recognition of these characteristic changes in the organization of collagen fiber may potentially serve as an early diagnostic marker in various pathological processes, such as hyperplastic, dysplastic, and cancerous tissues. This review focuses on the physiological and pathological orientation of collagen fibers in relation to epithelium that acts as an image-based biomarker. How to cite this article Pavithra V, Sowmya SV, Rao RS, Patil S, Augustine D, Haragannavar VC, Nambiar S. Tumorassociated Collagen Signatures: An Insight. World J Dent 2017;8(3):224-230.

Development of anin vitro extracellular matrix assay for studies of brain tumor cell invasion

1994 ◽  
Vol 20 (1) ◽  
pp. 1-15 ◽  
Author(s):  
Arun P. Amar ◽  
Stephen J. DeArmond ◽  
Donna R. Spencer ◽  
Peter F. Coopersmith ◽  
Daniel M. Ramos ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Brain Tumor ◽  
Tumor Cell ◽  
Cell Invasion ◽  
Tumor Cell Invasion ◽  
Brain Tumor Cell

scholarly journals Epidermal Growth Factor-Induced Tumor Cell Invasion and Metastasis Initiated by Dephosphorylation and Downregulation of Focal Adhesion Kinase

2001 ◽  
Vol 21 (12) ◽  
pp. 4016-4031 ◽  
Author(s):  
Zhimin Lu ◽  
Guoqiang Jiang ◽  
Peter Blume-Jensen ◽  
Tony Hunter
Keyword(s):  
Extracellular Matrix ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Tumor Cell ◽  
Focal Adhesion ◽  
Cell Invasion ◽  
Tumor Cell Invasion ◽  
Invasion And Metastasis ◽  
Autocrine Regulation ◽  
Epidermal Growth

ABSTRACT Upregulated epidermal growth factor (EGF) receptor (EGFR) expression and EGFR-induced signaling have been correlated with progression to invasion and metastasis in a wide variety of carcinomas, but the mechanism behind this is not well understood. We show here that, in various human carcinoma cells that overexpress EGFR, EGF treatment induced rapid tyrosine dephosphorylation of focal adhesion kinase (FAK) associated with downregulation of its kinase activity. The downregulation of FAK activity was both required and sufficient for EGF-induced refractile morphological changes, detachment of cells from the extracellular matrix, and increased tumor cell motility, invasion, and metastasis. Tumor cells with downregulated FAK activity became less adherent to the extracellular matrix. However, once cells started reattaching, FAK activity was restored by activated integrin signaling. Moreover, this process of readhesion and spreading could not be abrogated by further EGF stimulation. Interruption of transforming growth factor alpha-EGFR autocrine regulation with an EGFR tyrosine kinase inhibitor led to a substantial increase in FAK tyrosine phosphorylation and inhibition of tumor cell invasion in vitro. Consistent with this, FAK tyrosine phosphorylation was reduced in cells from tumors growing in transplanted, athymic, nude mice, which have an intact autocrine regulation of the EGFR. We suggest that the dynamic regulation of FAK activity, initiated by EGF-induced downregulation of FAK leading to cell detachment and increased motility and invasion, followed by integrin-dependent reactivation during readhesion, plays a role in EGF-associated tumor invasion and metastasis.

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