ERK activation and nuclear signaling induced by the loss of cell/matrix adhesion stimulates anchorage-independent growth of ovarian cancer cells

2008 ◽  
Vol 105 (3) ◽  
pp. 875-884 ◽  
Author(s):  
Adnan Al-Ayoubi ◽  
Adel Tarcsafalvi ◽  
Hui Zheng ◽  
Wayne Sakati ◽  
Scott T. Eblen
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Ovarian Cancer Cells ◽  
Erk Activation ◽  
Anchorage Independent Growth ◽  
Nuclear Signaling ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Cell Matrix Adhesion

Ezrin regulates cell-cell and cell-matrix adhesion, a possible role with E-cadherin/beta-catenin

1999 ◽  
Vol 112 (18) ◽  
pp. 3081-3090 ◽  
Author(s):  
S. Hiscox ◽  
W.G. Jiang
Keyword(s):  
Cancer Cells ◽  
Focal Adhesions ◽  
Beta Catenin ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Ezrin Expression ◽  
Coated Surfaces ◽  
Cell Matrix Adhesion ◽  
E Cadherin ◽  
Cell Cell

Ezrin, radixin, moesin and merlin form a subfamily of conserved proteins in the band 4.1 superfamily. The function of these proteins is to link the plasma membrane to the actin cytoskeleton. Merlin is defective or absent in schwannomas and meningiomas and has been suggested to function as a tumour suppressor. In this study, we have examined the role of ezrin as a potential regulator of the adhesive and invasive behaviour of tumour cells. We have shown that following inhibition of ezrin expression in colo-rectal cancer cells using antisense oligonucleotides, these cells displayed a reduced cell-cell adhesiveness together with a gain in their motile and invasive behaviour. These cells also displayed increased spreading over matrix-coated surfaces. Immunofluorescence studies revealed that antisense-treated cells also displayed an increased staining of paxillin in areas representing focal adhesions. Furthermore, coprecipitation studies revealed an association of ezrin with E-cadherin and beta-catenin. Induction of the phosphorylation of ezrin by orthovanadate and hepatocyte growth factor/scatter factor resulted in changes similar to those seen with antisense treatment, together with a marked decrease in the association of ezrin with both beta-catenin and E-cadherin. It is concluded that ezrin regulates cell-cell and cell-matrix adhesion, by interacting with cell adhesion molecules E-cadherin and beta-catenin, and may thus play an important role in the control of adhesion and invasiveness of cancer cells.

MATHEMATICAL MODELLING OF CANCER INVASION: THE IMPORTANCE OF CELL–CELL ADHESION AND CELL–MATRIX ADHESION

2011 ◽  
Vol 21 (04) ◽  
pp. 719-743 ◽  
Author(s):  
MARK A. J. CHAPLAIN ◽  
MIROSŁAW LACHOWICZ ◽  
ZUZANNA SZYMAŃSKA ◽  
DARIUSZ WRZOSEK
Keyword(s):  
Extracellular Matrix ◽  
Cell Adhesion ◽  
Cancer Cells ◽  
Classical Solutions ◽  
Invasion Process ◽  
Open Problems ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Cell Matrix Adhesion ◽  
Cell Cell

The process of invasion of tissue by cancer cells is crucial for metastasis — the formation of secondary tumours — which is the main cause of mortality in patients with cancer. In the invasion process itself, adhesion, both cell–cell and cell–matrix, plays an extremely important role. In this paper, a mathematical model of cancer cell invasion of the extracellular matrix is developed by incorporating cell–cell adhesion as well as cell–matrix adhesion into the model. Considering the interactions between cancer cells, extracellular matrix and matrix degrading enzymes, the model consists of a system of reaction–diffusion partial integro–differential equations, with nonlocal (integral) terms describing the adhesive interactions between cancer cells and the host tissue, i.e. cell–cell adhesion and cell–matrix adhesion. Having formulated the model, we prove the existence and uniqueness of global in time classical solutions which are uniformly bounded. Then, using computational simulations, we investigate the effects of the relative importance of cell–cell adhesion and cell–matrix adhesion on the invasion process. In particular, we examine the roles of cell–cell adhesion and cell–matrix adhesion in generating heterogeneous spatio-temporal solutions. Finally, in the discussion section, concluding remarks are made and open problems are indicated.

scholarly journals Correction to: FAK-ERK activation in cell/matrix adhesion induced by the loss of apolipoprotein E stimulates the malignant progression of ovarian cancer

2019 ◽  
Vol 38 (1) ◽  
Author(s):  
Huiling Lai ◽  
Xuejiao Zhao ◽  
Yu Qin ◽  
Yi Ding ◽  
Ruqi Chen ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Treatment Group ◽  
Apolipoprotein E ◽  
Malignant Progression ◽  
Original Publication ◽  
Erk Activation ◽  
Cell Matrix ◽  
Pre Treatment ◽  
Cell Matrix Adhesion ◽  
Corrected Figure

In the original publication of this manuscript [1], Fig. 5E lower panel was incorrect due to an error in the preparation of these figures for publication. It was noticed that in the lower panel of Fig. 5E, one mouse image of ApoE−/− + PBS group (upper) was a photograph coming from ApoE−/− + BAPN pre-treatment group (lower). The corrected figure appears below. We apologize for any confusion this may have caused.

scholarly journals CASP4 gene silencing in epithelial cancer cells leads to impairment of cell migration, cell-matrix adhesion and tissue invasion

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Giuliana Papoff ◽  
Dario Presutti ◽  
Cristiana Lalli ◽  
Giulia Bolasco ◽  
Simonetta Santini ◽  
...  
Keyword(s):  
Cell Migration ◽  
Gene Silencing ◽  
Cancer Cells ◽  
Epithelial Cancer ◽  
Tissue Invasion ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Cell Matrix Adhesion
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