Individual cell-based models of cell scatter of ARO and MLP-29 cells in response to hepatocyte growth factor

Scianna, Marco; Merks, Roeland; Preziosi, Luigi; Medico, Enzo

doi:10.1016/j.jtbi.2009.05.017

Cited by 17 publications

(10 citation statements)

References 32 publications

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“…Glioma cell’s motility is also influenced by various chemoattractants, which include ligands of scatter factor/hepatocyte growth factor (SF/HGF) (Lamszus et al, 1998), the EGF family (Lund-Johansen et al, 1990), the TGF- β family (Platten et al, 2001), SDF-1 (Zhou et al, 2002), and certain lipids (Young and Brocklyn, 2007). We note that other authors studied the action of HGF or scatter factor on cell migration (Tamagnone and Comoglio, 1997; Luca et al, 1999; Stella and Comoglio, 1999; Trusolino and Comoglio, 2002; Scianna et al, 2009). Beside these factors, other cell types such as microglia can also provide indirect stimulation of cell migration by secreting matrix components and chemoattractants (Watters et al, 2005).…”

Section: Introductionmentioning

confidence: 66%

Regulation of Cell Proliferation and Migration in Glioblastoma: New Therapeutic Approach

Kim

2013

Front. Oncol.

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Glioblastoma is the most aggressive brain cancer with the poor survival rate. A microRNA, miR-451, and its downstream molecules, CAB39/LKB1/STRAD/AMPK, are known to play a critical role in regulating a biochemical balance between rapid proliferation and invasion in the presence of metabolic stress in microenvironment. We develop a novel multi-scale mathematical model where cell migration and proliferation are controlled through a core intracellular control system (miR-451-AMPK complex) in response to glucose availability and physical constraints in the microenvironment. Tumor cells are modeled individually and proliferation and migration of those cells are regulated by the intracellular dynamics and reaction-diffusion equations of concentrations of glucose, chemoattractant, extracellular matrix, and MMPs. The model predicts that invasion patterns and rapid growth of tumor cells after conventional surgery depend on biophysical properties of cells, dynamics of the core control system, and microenvironment as well as glucose injection methods. We developed a new type of therapeutic approach: effective injection of chemoattractant to bring invasive cells back to the surgical site after initial surgery, followed by glucose injection at the same location. The model suggests that a good combination of chemoattractant and glucose injection at appropriate time frames may lead to an effective therapeutic strategy of eradicating tumor cells.

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Section: Introductionmentioning

confidence: 66%

Regulation of Cell Proliferation and Migration in Glioblastoma: New Therapeutic Approach

Kim

2013

Front. Oncol.

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“…The CPM method is becoming an increasingly common technique for the mathematical modeling of a wide range of biological phenomena, including avascular and vascular tumor growth [58][59][60][61] , gastrulation [62] , skin pigmentation [63] , yeast colony growth [64] , stem cell differentiation [65] , fruiting body formation of Dictyostelium discoideum [66] , epidermal formation [67] , hydra regeneration [66] , retinal patterning [68] , wound healing [69,70] , biofilms [71] , chick limb-bud growth [72][73][74] , cellular differentiation and growth of tissues, blood flow and thrombus development [75][76][77] , angiogenesis [70,[78][79][80][81] , dynamics of vascular cells [82][83][84][85] , cell scattering [86] , cell migration on and within matrix environments [56,57,87] . Notably, in [88] the authors introduced a compartmentalized approach to subdivide a Myxococcus xanthus into strings of subcellular domains with different rigidity, this in order to give the bacterium a particular geometry and to control its overall length.…”

Section: Discussionmentioning

confidence: 99%

A Cellular Potts Model of single cell migration in presence of durotaxis

Allena

Scianna

Preziosi

2016

Mathematical Biosciences

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Cell migration is a fundamental biological phenomenon during which cells sense their surroundings and respond to different types of signals. In presence of durotaxis, cells preferentially crawl from soft to stiff substrates by reorganizing their cytoskeleton from an isotropic to an anisotropic distribution of actin filaments. In the present paper, we propose a Cellular Potts Model to simulate single cell migration over flat substrates with variable stiffness. We have tested five configurations: (i) a substrate including a soft and a stiff region, (ii) a soft substrate including two parallel stiff stripes, (iii) a substrate made of successive stripes with increasing stiffness to create a gradient and (iv) a stiff substrate with four embedded soft squares. For each simulation, we have evaluated the morphology of the cell, the distance covered, the spreading area and the migration speed. We have then compared the numerical results to specific experimental observations showing a consistent agreement.

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“…Rubenstein and Kaufman [458] recently studied the role of ECM in glioma invasion using a version of the GGH model. Scianna et al [473] used the GGH model to simulate cell scatter in MLP-29 mouse embryo liver cell tumours in response to hepatocyte growth factor. Very recently, Poplawski et al [422] studied the morphological evolution of 2D avascular tumours using the GGH model and developed a phase diagram characterizing the development of instabilities at the tumour/host interface and tumour morphologies with critical parameters measuring diffusional limitations (ratio of growth rate to diffusion rate) and cell–cell adhesiveness.…”

Section: Discrete Modellingmentioning

confidence: 99%

Nonlinear modelling of cancer: bridging the gap between cells and tumours

et al. 2009

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Despite major scientific, medical and technological advances over the last few decades, a cure for cancer remains elusive. The disease initiation is complex, and including initiation and avascular growth, onset of hypoxia and acidosis due to accumulation of cells beyond normal physiological conditions, inducement of angiogenesis from the surrounding vasculature, tumour vascularization and further growth, and invasion of surrounding tissue and metastasis. Although the focus historically has been to study these events through experimental and clinical observations, mathematical modelling and simulation that enable analysis at multiple time and spatial scales have also complemented these efforts. Here, we provide an overview of this multiscale modelling focusing on the growth phase of tumours and bypassing the initial stage of tumourigenesis. While we briefly review discrete modelling, our focus is on the continuum approach. We limit the scope further by considering models of tumour progression that do not distinguish tumour cells by their age. We also do not consider immune system interactions nor do we describe models of therapy. We do discuss hybrid-modelling frameworks, where the tumour tissue is modelled using both discrete (cell-scale) and continuum (tumour-scale) elements, thus connecting the micrometre to the centimetre tumour scale. We review recent examples that incorporate experimental data into model parameters. We show that recent mathematical modelling predicts that transport limitations of cell nutrients, oxygen and growth factors may result in cell death that leads to morphological instability, providing a mechanism for invasion via tumour fingering and fragmentation. These conditions induce selection pressure for cell survivability, and may lead to additional genetic mutations. Mathematical modelling further shows that parameters that control the tumour mass shape also control its ability to invade. Thus, tumour morphology may serve as a predictor of invasiveness and treatment prognosis.

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Individual cell-based models of cell scatter of ARO and MLP-29 cells in response to hepatocyte growth factor

Cited by 17 publications

References 32 publications

Regulation of Cell Proliferation and Migration in Glioblastoma: New Therapeutic Approach

Regulation of Cell Proliferation and Migration in Glioblastoma: New Therapeutic Approach

A Cellular Potts Model of single cell migration in presence of durotaxis

Nonlinear modelling of cancer: bridging the gap between cells and tumours

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