Silencing of Mig-7 expression inhibits in-vitro invasiveness and vasculogenic mimicry of human glioma U87 Cells

Background: Vasculogenic mimicry (VM) is an adaptive biological phenomenon wherein cancer cells spontaneously self-organize into 3-dimensional (3D) branching network structures. This emergent behavior is considered central in promoting an invasive, metastatic, and therapy resistance molecular signature to cancer cells. The quantitative analysis of such complex phenotypic systems could require the use of computational approaches including machine learning algorithms originating from complexity science. Procedures: In vitro 3D VM was performed with SKOV3 and ES2 ovarian cancer cells cultured on Matrigel. Diet-derived catechins disruption of VM was monitored at 24 hours with pictures taken with an inverted microscope. Three computational algorithms for complex feature extraction relevant for 3D VM, including 2D wavelet analysis, fractal dimension, and percolation clustering scores were assessed coupled with machine learning classifiers. Results: These algorithms demonstrated the structure-to-function galloyl moiety impact on VM for each of the gallated catechin tested, and shown applicable in quantifying the drug-mediated structural changes in VM processes. Conclusions: Our study provides evidence of how appropriate 3D VM compression and feature extractors coupled with classification/regression methods could be efficient to study in vitro drug-induced perturbation of complex processes. Such approaches could be exploited in the development and characterization of drugs targeting VM.

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CD36 promotes vasculogenic mimicry in melanoma by mediating adhesion to the extracellular matrix

BMC Cancer ◽

10.1186/s12885-021-08482-4 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Carmela Martini ◽

Mark DeNichilo ◽

Danielle P. King ◽

Michaelia P. Cockshell ◽

Brenton Ebert ◽

...

Keyword(s):

Extracellular Matrix ◽

Cancer Cells ◽

Vasculogenic Mimicry ◽

Tumor Vasculature ◽

Melanoma Cells ◽

Human Melanoma ◽

Cell Surface Glycoprotein ◽

Melanoma Cancer ◽

In Vitro Angiogenesis

Abstract Background The formation of blood vessels within solid tumors directly contributes to cancer growth and metastasis. Until recently, tumor vasculature was thought to occur exclusively via endothelial cell (EC) lined structures (i.e. angiogenesis), but a second source of tumor vasculature arises from the cancer cells themselves, a process known as vasculogenic mimicry (VM). While it is generally understood that the function of VM vessels is the same as that of EC-lined vessels (i.e. to supply oxygen and nutrients to the proliferating cancer cells), the molecular mechanisms underpinning VM are yet to be fully elucidated. Methods Human VM-competent melanoma cell lines were examined for their VM potential using the in vitro angiogenesis assays (Matrigel), together with inhibition studies using small interfering RNA and blocking monoclonal antibodies. Invasion assays and adhesion assays were used to examine cancer cell function. Results Herein we demonstrate that CD36, a cell surface glycoprotein known to promote angiogenesis by ECs, also supports VM formation by human melanoma cancer cells. In silico analysis of CD36 expression within the melanoma cohort of The Cancer Genome Atlas suggests that melanoma patients with high expression of CD36 have a poorer clinical outcome. Using in vitro ‘angiogenesis’ assays and CD36-knockdown approaches, we reveal that CD36 supports VM formation by human melanoma cells as well as adhesion to, and invasion through, a cancer derived extracellular matrix substrate. Interestingly, thrombospondin-1 (TSP-1), a ligand for CD36 on ECs that inhibits angiogenesis, has no effect on VM formation. Further investigation revealed a role for laminin, but not collagen or fibronectin, as ligands for CD36 expressing melanoma cells. Conclusions Taken together, this study suggests that CD36 is a novel regulator of VM by melanoma cancer cells that is facilitated, at least in part, via integrin-α3 and laminin. Unlike angiogenesis, VM is not perturbed by the presence of TSP-1, thus providing new information on differences between these two processes of tumor vascularization which may be exploited to combat cancer progression.

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Metastasis tumor-associated protein-2 knockdown suppresses the proliferation and invasion of human glioma cells in vitro and in vivo

Journal of Neuro-Oncology ◽

10.1007/s11060-014-1558-3 ◽

2014 ◽

Vol 120 (2) ◽

pp. 273-281 ◽

Cited By ~ 15

Author(s):

Chun-Yuan Cheng ◽

Ying-Erh Chou ◽

Chung-Po Ko ◽

Shun-Fa Yang ◽

Shu-Ching Hsieh ◽

...

Keyword(s):

Glioma Cells ◽

Human Glioma ◽

Human Glioma Cells ◽

Proliferation And Invasion

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Oligosaccharide G19 inhibits U-87 MG human glioma cells growth in vitro and in vivo by targeting epidermal growth factor (EGF) and activating p53/p21 signaling

Glycobiology ◽

10.1093/glycob/cwu038 ◽

2014 ◽

Vol 24 (8) ◽

pp. 748-765 ◽

Cited By ~ 9

Author(s):

Hailing Liu ◽

Ling Zhou ◽

Songshan Shi ◽

Ying Wang ◽

Xinyan Ni ◽

...

Keyword(s):

Growth Factor ◽

Epidermal Growth Factor ◽

Glioma Cells ◽

Human Glioma ◽

Human Glioma Cells ◽

Epidermal Growth

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B16 melanoma secretomes and in vitro invasiveness: syntenin as an invasion modulator

Melanoma Research ◽

10.1097/cmr.0b013e32833279f2 ◽

2010 ◽

Vol 20 (2) ◽

pp. 77-84 ◽

Cited By ~ 9

Author(s):

Fabien Rondepierre ◽

Bernadette Bouchon ◽

Mathilde Bonnet ◽

Nicole Moins ◽

Jean M. Chezal ◽

...

Keyword(s):

B16 Melanoma ◽

In Vitro Invasiveness

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P13.23 Study of migration characteristics of human glioma cells in vitro

Neuro-Oncology ◽

10.1093/neuonc/noab180.129 ◽

2021 ◽

Vol 23 (Supplement_2) ◽

pp. ii37-ii38

Author(s):

G Pavlova ◽

S Pavlova ◽

S Drozd ◽

E Savchenko ◽

L Zakharova ◽

...

Keyword(s):

Cell Cultures ◽

Proliferative Activity ◽

Average Rate ◽

Glioma Cells ◽

Human Glioma ◽

Human Gliomas ◽

Migration Activity ◽

Tumor Invasiveness ◽

Grade Iii

Abstract BACKGROUND Gliomas are still one of the most aggressive human cancers, and even despite modern therapeutic approaches, the prognosis for patients with this disease is not favorable. It is known that glioma cells are capable of local invasiveness, when glioma cells migrate into healthy brain tissue. A lack of any definite markers, characterizing migrating glioma cells and allowing them to be distinguished from healthy brain cells, requires a thorough investigation. In case it would be possible to characterize invasive glioma cells, then a development of targeted therapy could be feasible. MATERIAL AND METHODS Cell cultures of human gliomas Gr II, III and IV were developed with 5 cultures for each Grade. MTT, RT-PCR, Western and Nosern blot, transcriptome analysis were applied. RESULTS Three cultures of human gliomas had a high degree of migration, within the range of 6% - 14%. These cultures were developed from gliomas of Grade III and Grade IV, and with IDH1- (minus) phenotype. Moreover, cell cultures with IDH1 + (plus) phenotype had a low migration rate within 1%. An intensity of migration correlated with the degree of malignancy, and an average rate decreased with a decrease of the Grade. Moreover, an analysis of the proliferative activity of cell cultures of human gliomas of various degrees of malignancy did not reveal a relationship with a migratory properties of cultures. A number of actively proliferating cultures did not show high migration, while cultures with medium proliferative activity could show a high level of migration. The low level of proliferation of cultures of gliomas of Grade II and I at the beginning of cultivation, in some cases, subsequently increased, but an inherent low migration activity did not change. In actively migrating cultures, a significant decrease in the expression of Sox2 and Nestin is detected. A positive correlation was found between migration abilities of human glioma cell culture cells and the marker Ki67, GFAP, Sox2, and Oct4. The difference was statistically significant by the one-sided Mann-Whitney test. CONCLUSION Conclusions: Cell cultures derived from glioma tumor tissue can be used to predict invasive properties of the tumor. High tumor invasiveness is characteristic for Grade III and Grade IV, and with IDH1- (minus) phenotype, and it also correlates with elevated expression of GFAP, Sox2 and Oct4The reported study was funded by RFBR according to the research project № 18-29-01012 and by the Ministry of Science and Higher Education of the Russian Federation, grant number 075-15-2020-809 (13.1902.21.0030).

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