Spontaneous formation and spatial self-organization of mechanically induced mesenchymal-like cells within geometrically confined cancer cell monolayers

Biomaterials ◽  
2021 ◽  
pp. 121337
Author(s):  
Feng Lin ◽  
Yuwei Zhou ◽  
Xiaocen Duan ◽  
Xu Fang ◽  
Qing Zhang ◽  
...  
Keyword(s):  
Cancer Cell ◽  
Self Organization ◽  
Cell Monolayers ◽  
Spontaneous Formation ◽  
Geometrically Confined

scholarly journals Combined Effects of Gold Nanoparticles and Ionizing Radiation on Human Prostate and Lung Cancer Cell Migration

2019 ◽  
Vol 20 (18) ◽  
pp. 4488 ◽  
Author(s):  
Elham Shahhoseini ◽  
Bryce N. Feltis ◽  
Masao Nakayama ◽  
Terrence J. Piva ◽  
Dodie Pouniotis ◽  
...  
Keyword(s):  
Gold Nanoparticles ◽  
Cell Migration ◽  
Ionizing Radiation ◽  
Cell Lines ◽  
Cancer Cell ◽  
A549 Cells ◽  
Human Prostate ◽  
Cell Monolayers ◽  
Altered Cell ◽  
Relative Migration

The effect of 15 nm-sized gold nanoparticles (AuNPs) and/or ionizing radiation (IR) on the migration and adhesion of human prostate (DU145) and lung (A549) cancer cell lines was investigated. Cell migration was measured by observing the closing of a gap created by a pipette tip on cell monolayers grown in 6-well plates. The ratio of the gap areas at 0 h and 24 h were used to calculate the relative migration. The relative migration of cells irradiated with 5 Gy was found to be 89% and 86% for DU145 and A549 cells respectively. When the cells were treated with 1 mM AuNPs this fell to ~75% for both cell lines. However, when the cells were treated with both AuNPs and IR an additive effect was seen, as the relative migration rate fell to ~60%. Of interest was that when the cells were exposed to either 2 or 5 Gy IR, their ability to adhere to the surface of a polystyrene culture plate was significantly enhanced, unlike that seen for AuNPs. The delays in gap filling (cell migration) in cells treated with IR and/or AuNPs can be attributed to cellular changes which also may have altered cell motility. In addition, changes in the cytoskeleton of the cancer cells may have also affected adhesiveness and thus the cancer cell’s motility response to IR.

scholarly journals Oceanic Rings and Jets as Statistical Equilibrium States

2011 ◽  
Vol 41 (10) ◽  
pp. 1860-1873 ◽  
Author(s):  
Antoine Venaille ◽  
Freddy Bouchet
Keyword(s):  
Coherent Structures ◽  
Large Scale ◽  
Wind Forcing ◽  
Statistical Equilibrium ◽  
Self Organization ◽  
Equilibrium Studies ◽  
Spontaneous Formation ◽  
Basin Scale ◽  
Quasigeostrophic Model ◽  
Unstable States

Abstract Equilibrium statistical mechanics of two-dimensional flows provides an explanation and a prediction for the self-organization of large-scale coherent structures. This theory is applied in this paper to the description of oceanic rings and jets, in the framework of a 1.5-layer quasigeostrophic model. The theory predicts the spontaneous formation of regions where the potential vorticity is homogenized, with strong and localized jets at their interface. Mesoscale rings are shown to be close to a statistical equilibrium: the theory accounts for their shape, drift, and ubiquity in the ocean, independently of the underlying generation mechanism. At basin scale, inertial states presenting midbasin eastward jets (and then different from the classical Fofonoff solution) are described as marginally unstable states. In that case, considering a purely inertial limit is a first step toward more comprehensive out-of-equilibrium studies that would take into account other essential aspects, such as wind forcing.

scholarly journals Tissue-Engineered Bone Tumor as a Reproducible Human in Vitro Model for Studies of Anticancer Drugs

2019 ◽  
Author(s):  
Courtney Sakolish ◽  
John S House ◽  
Alan Chramiec ◽  
Yizhong Liu ◽  
Zunwei Chen ◽  
...  
Keyword(s):  
Anticancer Drugs ◽  
Cancer Cell ◽  
Bone Tumor ◽  
Tumor Model ◽  
Drug Binding ◽  
Human Bone ◽  
Preclinical Studies ◽  
Es Cell ◽  
Combination Drug ◽  
Cell Monolayers

Abstract Studies of anticancer therapies in traditional cell culture models can demonstrate efficacy of direct-acting compounds but lack the 3-dimensional arrangement of the tumor cells and their tissue-specific microenvironments, both of which are important modulators of treatment effects in vivo. Bone cells reside in complex environments that regulate their fate and function. A bioengineered human bone-tumor model has been shown to provide a microphysiological niche for studies of cancer cell behavior. Here, we demonstrate successful transfer between 2 laboratories and utility of this model in efficacy studies using well-established chemotherapeutic agents. The bioengineered human bone-tumor model consisted of Ewing sarcoma (RD-ES) cancer cell aggregates infused into tissue-engineered bone that was grown from human mesenchymal stem cell-derived differentiated into osteoblasts within mineralized bone scaffolds. The tumor model was maintained in culture for over 5 weeks and subjected to clinically relevant doses of linsitinib, doxorubicin, cisplatin, methotrexate, vincristine, dexamethasone, or MAP (methotrexate, doxorubicin, and cisplatin combination). Drug administration cycles were designed to mimic clinical treatment regimens. The bioengineered tumors were evaluated days to weeks after the cessation of treatment to monitor the potential for relapse, using bioengineered bone and ES cell monolayers as controls. Drug binding to the scaffolds and media proteins and gene expression were also evaluated. We show that a bioengineered human bone tumor can be used as a microphysiological model for preclinical studies of anticancer drugs. We found that anticancer efficacy was achieved at concentrations approximating the human Cmax, in contrast to traditional ES cell monolayers. These studies show that the bone-tumor model can be successfully transferred between laboratories and has predictive power in preclinical studies. The effects of drugs on the bone tumors and healthy bone were studied in parallel, in support of the utility of this model for identification of new therapeutic targets.

Cytotoxicity of PAI2, C595 and Herceptin vectors labeled with the alpha-emitting radioisotope Bismuth-213 for ovarian cancer cell monolayers and clusters

2006 ◽  
Vol 234 (2) ◽  
pp. 176-183 ◽  
Author(s):  
Yan J. Song ◽  
Chang F. Qu ◽  
Syed M.A. Rizvi ◽  
Yong Li ◽  
G. Robertson ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Cell Monolayers

Transient upregulation of GRP and its receptor critically regulate colon cancer cell motility during remodeling

2005 ◽  
Vol 288 (6) ◽  
pp. G1274-G1282 ◽  
Author(s):  
Sarah Glover ◽  
Rajkumar Nathaniel ◽  
Lubna Shakir ◽  
Cecile Perrault ◽  
Rebecca K. Anderson ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Motility ◽  
Cancer Cell ◽  
Human Colon ◽  
Colon Cancer Cell ◽  
Human Colon Cancer ◽  
Cell Monolayers ◽  
Cancer Cell Motility ◽  
Cell Remodeling ◽  
Confluent Cell

Gastrin-releasing peptide (GRP) is typically viewed as a growth factor in cancer. However, we have suggested that in colon cancer, GRP acts primarily as a morphogen when it and its receptor (GRP-R) are aberrantly upregulated. As such, GRP/GRP-R act(s) primarily to modulate processes contributing to the assumption or maintenance of tumor differentiation. One of the most important such processes is the ability of tumor cells to achieve directed motility in the context of tissue remodeling. Yet the cellular conditions affecting GRP/GRP-R expression, and the biochemical pathways involved in mediating its morphogenic properties, remain to be established. To study this, we evaluated the human colon cancer cell lines Caco-2 and HT-29 cells. We found that confluent cells do not express GRP/GRP-R. In contrast, disaggreation and plating at subconfluent densities results in rapid GRP/GRP-R upregulation followed by their progressive decrease as confluence is achieved. GRP/GRP-R coexpression correlated with that of focal adhesion kinase (FAK) phosphorylation of Tyr397, Tyr407, Tyr861, and Tyr925 but not Tyr576 or Tyr577. To more specifically evaluate the kinetics of GRP/GRP-R upregulation, we wounded confluent cell monolayers. At t = 0 h GRP/GRP-R were not expressed, yet cells immediately began migrating into the gap created by the wound. GRP/GRP-R were first detected at ∼2 h, and maximal levels were observed at ∼6 h postwounding. The GRP-specific antagonist [d-Phe6]-labeled bombesin methyl ester had no effect on cell motility before GRP-R expression. In contrast, this agent increasingly attenuated cell motility with increasing GRP-R expression such that from t = 6 h onward no further cell migration into the gap was observed. Overall, these findings indicate the existence of GRP-independent and -dependent phases of tumor cell remodeling with the latter mediating colon cancer cell motility during remodeling via FAK.

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