scholarly journals A Human Glioblastoma Organotypic Slice Culture Model for Study of Tumor Cell Migration and Patient-specific Effects of Anti-Invasive Drugs

10.3791/53557 ◽  
2017 ◽  
Author(s):  
Jonathon J. Parker ◽  
Marcela Lizarraga ◽  
Allen Waziri ◽  
Kara M. Foshay
Keyword(s):  
Cell Migration ◽  
Tumor Cell ◽  
Patient Specific ◽  
Slice Culture ◽  
Human Glioblastoma ◽  
Tumor Cell Migration ◽  
Organotypic Slice Culture ◽  
Specific Effects ◽  
Culture Model

scholarly journals Gefitinib selectively inhibits tumor cell migration in EGFR-amplified human glioblastoma

2013 ◽  
Vol 15 (8) ◽  
pp. 1048-1057 ◽  
Author(s):  
J. J. Parker ◽  
K. R. Dionne ◽  
R. Massarwa ◽  
M. Klaassen ◽  
N. K. Foreman ◽  
...  
Keyword(s):  
Cell Migration ◽  
Tumor Cell ◽  
Human Glioblastoma ◽  
Tumor Cell Migration

scholarly journals A Novel 3D Co-culture Platform for Integrating Tissue Interfaces for Tumor Growth, Migration and Therapeutic Sensitivity: PP-3D-S

2021 ◽  
Author(s):  
Mansoureh Mohseni Garakani ◽  
Pouyan Ahangar ◽  
Sean Watson ◽  
Bernard Nisol ◽  
Michael R. Wertheimer ◽  
...  
Keyword(s):  
Cell Migration ◽  
Tumor Growth ◽  
Tumor Cell ◽  
Human Cancer ◽  
Patient Specific ◽  
Cancer Microenvironment ◽  
Tumor Cell Migration ◽  
Screening Experiments ◽  
Significant Difference

Metastatic cancers can be highly heterogeneous, show large patient variability, and are typically hard to treat due to chemoresistance. Personalized therapies are therefore needed to suppress tumor growth and enhance patient's quality of life. Identifying appropriate patient-specific therapies remains a challenge though, due mainly to non-physiological in vitro culture systems. Therefore, more complex and physiological in vitro human cancer microenvironment tools could drastically aid in the development of new therapies. We developed a plasma-modified, electro-spun 3D scaffold (PP-3D-S) that can mimic the human cancer microenvironment for customized-cancer therapeutic screening. The PP-3D-S were characterized for optimal plasma-modifying treatment and scaffolds morphology including fiber diameter and pore size. PP-3D-S was then seeded with human fibroblasts to mimic a stromal tissue layer; cell adhesion on plasma-modified poly (lactic acid), PLA, electrospun mats vastly exceeded that on untreated controls. The cell-seeded scaffolds were then overlaid with alginate/gelatin-based hydrogel embedded with MDA-MB231 human breast cancer cells, representing a tumor-tissue interface. Among three different plasma treatments, we found that NH3 plasma promoted the most tumor cell migration to the scaffold surfaces after 7 days of culture. For all treated and non-treated mats, we observed a significant difference in tumor cell migration between small-sized and either medium- or large-sized scaffolds. In addition, we found that the PP-3D-S was highly comparable to the standard Matrigel migration assays in two different sets of doxorubicin screening experiments, where a 75% reduction in migration was achieved with 0.5 uM doxorubicin for both systems. Taken together, our data indicate that PP-3D-S is an effective, low-cost, and easy-to-use alternate 3D tumor migration model which may be suitable as a physiological drug screening tool for personalized medicine against metastatic cancers.

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.

scholarly journals Compensation mechanism in tumor cell migration

2003 ◽  
Vol 160 (2) ◽  
pp. 267-277 ◽  
Author(s):  
Katarina Wolf ◽  
Irina Mazo ◽  
Harry Leung ◽  
Katharina Engelke ◽  
Ulrich H. von Andrian ◽  
...  
Keyword(s):  
Cell Migration ◽  
Tumor Cell ◽  
Shape Change ◽  
Proteolytic Degradation ◽  
Amoeboid Movement ◽  
Tumor Cell Migration ◽  
Tumor Dissemination ◽  
Β1 Integrins

Invasive tumor dissemination in vitro and in vivo involves the proteolytic degradation of ECM barriers. This process, however, is only incompletely attenuated by protease inhibitor–based treatment, suggesting the existence of migratory compensation strategies. In three-dimensional collagen matrices, spindle-shaped proteolytically potent HT-1080 fibrosarcoma and MDA-MB-231 carcinoma cells exhibited a constitutive mesenchymal-type movement including the coclustering of β1 integrins and MT1–matrix metalloproteinase (MMP) at fiber bindings sites and the generation of tube-like proteolytic degradation tracks. Near-total inhibition of MMPs, serine proteases, cathepsins, and other proteases, however, induced a conversion toward spherical morphology at near undiminished migration rates. Sustained protease-independent migration resulted from a flexible amoeba-like shape change, i.e., propulsive squeezing through preexisting matrix gaps and formation of constriction rings in the absence of matrix degradation, concomitant loss of clustered β1 integrins and MT1-MMP from fiber binding sites, and a diffuse cortical distribution of the actin cytoskeleton. Acquisition of protease-independent amoeboid dissemination was confirmed for HT-1080 cells injected into the mouse dermis monitored by intravital multiphoton microscopy. In conclusion, the transition from proteolytic mesenchymal toward nonproteolytic amoeboid movement highlights a supramolecular plasticity mechanism in cell migration and further represents a putative escape mechanism in tumor cell dissemination after abrogation of pericellular proteolysis.

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