scholarly journals Thymidine phosphorylase in cancer cells stimulates human endothelial cell migration and invasion by the secretion of angiogenic factors

2011 ◽  
Vol 104 (7) ◽  
pp. 1185-1192 ◽  
Author(s):  
I V Bijnsdorp ◽  
F Capriotti ◽  
F A E Kruyt ◽  
N Losekoot ◽  
M Fukushima ◽  
...  
Keyword(s):  
Cell Migration ◽  
Endothelial Cell ◽  
Cancer Cells ◽  
Thymidine Phosphorylase ◽  
Angiogenic Factors ◽  
Endothelial Cell Migration ◽  
Human Endothelial Cell ◽  
Migration And Invasion ◽  
Cell Migration And Invasion

scholarly journals Transferrin Promotes Endothelial Cell Migration and Invasion: Implication in Cartilage Neovascularization

1997 ◽  
Vol 136 (6) ◽  
pp. 1375-1384 ◽  
Author(s):  
Mariella F. Carlevaro ◽  
Adriana Albini ◽  
Domenico Ribatti ◽  
Chiara Gentili ◽  
Roberto Benelli ◽  
...  
Keyword(s):  
Cell Migration ◽  
Endothelial Cell ◽  
Endothelial Cell Migration ◽  
Migration And Invasion ◽  
Endochondral Bone Formation ◽  
Endochondral Bone ◽  
Cell Migration And Invasion ◽  
Hypertrophic Cartilage ◽  
Different Sources

During endochondral bone formation, avascular cartilage differentiates to hypertrophic cartilage that then undergoes erosion and vascularization leading to bone deposition. Resting cartilage produces inhibitors of angiogenesis, shifting to production of angiogenic stimulators in hypertrophic cartilage. A major protein synthesized by hypertrophic cartilage both in vivo and in vitro is transferrin. Here we show that transferrin is a major angiogenic molecule released by hypertrophic cartilage. Endothelial cell migration and invasion is stimulated by transferrins from a number of different sources, including hypertrophic cartilage. Checkerboard analysis demonstrates that transferrin is a chemotactic and chemokinetic molecule. Chondrocyte-conditioned media show similar properties. Polyclonal anti-transferrin antibodies completely block endothelial cell migration and invasion induced by purified transferrin and inhibit the activity produced by hypertrophic chondrocytes by 50–70% as compared with controls. Function-blocking mAbs directed against the transferrin receptor similarly reduce the endothelial migratory response. Chondrocytes differentiating in the presence of serum produce transferrin, whereas those that differentiate in the absence of serum do not. Conditioned media from differentiated chondrocytes not producing transferrin have only 30% of the endothelial cell migratory activity of parallel cultures that synthesize transferrin. The angiogenic activity of transferrins was confirmed by in vivo assays on chicken egg chorioallantoic membrane, showing promotion of neovascularization by transferrins purified from different sources including conditioned culture medium. Based on the above results, we suggest that transferrin is a major angiogenic molecule produced by hypertrophic chondrocytes during endochondral bone formation.

scholarly journals Study of LBHD1 Expression with Invasion and Migration of Bladder Cancer

2019 ◽  
Vol 14 (1) ◽  
pp. 440-447
Author(s):  
Chunhui Dong ◽  
Yihui Liu ◽  
Guiping Yu ◽  
Xu Li ◽  
Ling Chen
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Tumor Antigens ◽  
Urinary Bladder Cancer ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Invasion And Migration ◽  
Bladder Cancer Cells

AbstractLBHD1 (C11ORF48) is one of the ten potential tumor antigens identified by immunoscreening the urinary bladder cancer cDNA library in our previous study. We suspect that its expression is associated with human bladder cancer. However, the exact correlation remains unclear. To address the potential functional relationship between LBHD1 and bladder cancer, we examined the LBHD1 expression at the mRNA and protein level in 5 different bladder cancer cell lines: J82, T24, 253J, 5637, and BLZ-211. LBHD1 high and low expressing cells were used to investigate the migration, invasion, and proliferation of bladder cancer cells following transfection of LBHD1 with siRNA and plasmids, respectively. Our experiment showed that the degree of gene expression was positively related to the migration and invasion of the cancer cells while it had little effect on cell proliferation. Knocking down LBHD1 expression with LBHD1 siRNA significantly attenuated cell migration and invasion in cultured bladder cancer cells, and overexpressing LBHD1 with LBHD1 cDNA plasmids exacerbated cell migration and invasion. Nevertheless, a difference in cell proliferation after transfection of LBHD1 siRNA and LBHD1 cDNA plasmids was not found. Our findings suggest that LBHD1 might play a role in cell migration and invasion.

scholarly journals CDX2 and Reg IV expression and correlation in gastric cancer

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Dandan Chai ◽  
Huifen Du ◽  
Kesheng Li ◽  
Xueliang Zhang ◽  
Xiaoqin Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Real Time ◽  
Real Time Pcr ◽  
Ectopic Expression ◽  
Rank Correlation ◽  
Migration And Invasion ◽  
Gastric Cancer Cells ◽  
Cell Migration And Invasion

Abstract Background Ectopic expression of CDX2 is associated with the development and progression of gastric cancer. Previous studies showed that CDX2 may be an upstream regulator of Reg IV expression in gastric cancer, and our previous report showed that Reg IV upregulated SOX9 expression and enhanced cell migration and invasion in gastric cancer cells. However, the regulatory roles of CDX2 have not been clarified in gastric cancer, and the correlation between CDX2 and Reg IV requires further study. Methods CDX2 and Reg IV were examined in gastric cancer specimens and paired adjacent tissues via real-time PCR and immunohistochemistry (IHC). The association between CDX2 and Reg IV was assessed using the χ2-test and Spearman’s rank correlation. To verify their relationship, knockdown and exogenous expression of CDX2 or Reg IV were performed in AGS and MKN-45 gastric cancer cells, and their expression was subsequently analyzed via a real-time PCR and western blotting. Wound-healing and Transwell assays were used to examine migration and invasion in AGS and MKN-45 cells following CDX2 silencing or overexpression. Results A positive correlation was observed between CDX2 and Reg IV expression at the mRNA and protein levels in gastric cancer tissues. CDX2 silencing significantly downregulated Reg IV expression, and CDX2 overexpression significantly upregulated Reg IV expression in AGS and MKN-45 cells. Neither Reg IV silencing nor overexpression had any effect on CDX2 protein expression in AGS or MKN-45 cells, even though both affected the expression of CDX2 mRNA. Functionally, CDX2 silencing significantly inhibited cell migration and invasion, and CDX2 overexpression significantly promoted cell migration and invasion in AGS and MKN-45 cells. Conclusions Our findings demonstrate that CDX2 expression was positively correlated with that of Reg IV in gastric cancer, and CDX2 promoted cell migration and invasion through upregulation of Reg IV expression in AGS and MKN-45 cells.

scholarly journals Sevoflurane represses the migration and invasion of gastric cancer cells by regulating forkhead box protein 3

2021 ◽  
Vol 49 (4) ◽  
pp. 030006052110059
Author(s):  
Fangfang Yong ◽  
Hemei Wang ◽  
Chao Li ◽  
Huiqun Jia
Keyword(s):  
Gastric Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Cell Lines ◽  
Migration And Invasion ◽  
Control Group ◽  
Gastric Cancer Cells ◽  
Cell Migration And Invasion ◽  
Forkhead Box ◽  
Induced Apoptosis

Objective Previous studies suggested that sevoflurane exerts anti-proliferative, anti-migratory, and anti-invasive effects on cancer cells. To determine the role of sevoflurane on gastric cancer (GC) progression, we evaluated its effects on the proliferation, migration, and invasion of SGC7901, AGS, and MGC803 GC cells. Methods GC cells were exposed to different concentrations of sevoflurane (1.7, 3.4, or 5.1% v/v). Cell viability, migration, and invasion were evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and Transwell assays. Immunohistochemical staining and immunoblotting were performed to analyze forkhead box protein 3 (FOXP3) protein expression in tissue specimens and cell lines, respectively. Results FOXP3 was downregulated in human GC specimens and cell lines. Functionally, FOXP3 overexpression significantly inhibited the proliferation, migration, and invasion of GC cells and accelerated their apoptosis. Moreover, sevoflurane significantly blocked GC cell migration and invasion compared with the findings in the control group. However, FOXP3 silencing neutralized sevoflurane-induced apoptosis and the inhibition of GC cell migration and invasion. Sevoflurane-induced apoptosis and the suppression of migration and invasion might be associated with FOXP3 overactivation in GC cells. Conclusions Sevoflurane activated FOXP3 and prevented GC progression via inhibiting cell migration and invasion in vitro.

scholarly journals A Mathematical Model of anIn VitroExperiment to Investigate Endothelial Cell Migration

2002 ◽  
Vol 4 (4) ◽  
pp. 251-270 ◽  
Author(s):  
M. J. Plank ◽  
B. D. Sleeman ◽  
P. F. Jones
Keyword(s):  
Mathematical Model ◽  
Cell Migration ◽  
Endothelial Cell ◽  
Blood Vessels ◽  
Three Dimensional ◽  
Cell Movement ◽  
Quantitative Model ◽  
Angiogenic Factors ◽  
Endothelial Cell Migration ◽  
Angiogenic Factor

Angiogenesis, the growth of new blood vessels from existing ones, is an important, yet not fully understood, process and is involved in diseases such as rheumatoid arthritis, diabetic retinopathy and solid tumour growth. Central to the process of angiogenesis are endothelial cells (EC), which line all blood vessels, and are capable of forming new capillaries by migration, proliferation and lumen formation. We construct a cell-based mathematical model of an experiment (Vernon, R.B. and Sage, E.H. (1999) “A novel, quantitative model for study of endothelial cell migration and sprout formation within three-dimensional collagen matrices”,Microvasc. Res.57, 118–133) carried out to assess the response of EC to various diffusible angiogenic factors, which is a crucial part of angiogenesis. The model for cell movement is based on the theory of reinforced random walks and includes both chemotaxis and chemokinesis. Three-dimensional simulations are run and the results correlate well with the experimental data. The experiment cannot easily distinguish between chemotactic and chemokinetic effects of the angiogenic factors. We, therefore, also run two-dimensional simulations of a hypothetical experiment, with a point source of angiogenic factor. This enables directed (gradient-driven) EC migration to be investigated independently of undirected (diffusion-driven) migration.

scholarly journals CRIF1 deficiency suppresses endothelial cell migration via upregulation of RhoGDI2

PLoS ONE ◽  
2021 ◽  
Vol 16 (8) ◽  
pp. e0256646
Author(s):  
Harsha Nagar ◽  
Seonhee Kim ◽  
Ikjun Lee ◽  
Su-Jeong Choi ◽  
Shuyu Piao ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Migration ◽  
Endothelial Cell ◽  
Signaling Pathway ◽  
Umbilical Vein ◽  
Vascular Endothelial Cell ◽  
Cellular Migration ◽  
Endothelial Cell Migration ◽  
Migration And Invasion ◽  
Mitochondrial Functions

Rho GDP-dissociation inhibitor (RhoGDI), a downregulator of Rho family GTPases, prevents nucleotide exchange and membrane association. It is responsible for the activation of Rho GTPases, which regulate a variety of cellular processes, such as migration. Although RhoGDI2 has been identified as a tumor suppressor gene involved in cellular migration and invasion, little is known about its role in vascular endothelial cell (EC) migration. CR6-interacting factor 1 (CRIF1) is a CR6/GADD45-interacting protein with important mitochondrial functions and regulation of cell growth. We examined the expression of RhoGDI2 in CRIF1-deficient human umbilical vein endothelial cells (HUVECs) and its role in cell migration. Expression of RhoGDI2 was found to be considerably higher in CRIF1-deficient HUVECs along with suppression of cell migration. Moreover, the phosphorylation levels of Akt and CREB were decreased in CRIF1-silenced cells. The Akt-CREB signaling pathway was implicated in the changes in endothelial cell migration caused by CRIF1 downregulation. In addition to RhoGDI2, we identified another factor that promotes migration and invasion of ECs. Adrenomedullin2 (ADM2) is an autocrine/paracrine factor that regulates vascular tone and other vascular functions. Endogenous ADM2 levels were elevated in CRIF1-silenced HUVECs with no effect on cell migration. However, siRNA-mediated depletion of RhoGDI2 or exogenous ADM2 administration significantly restored cell migration via the Akt-CREB signaling pathway. In conclusion, RhoGDI2 and ADM2 play important roles in the migration of CRIF1-deficient endothelial cells.

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