scholarly journals Tight Junctions: A Barrier to the Initiation and Progression of Breast Cancer?

2010 ◽  
Vol 2010 ◽  
pp. 1-16 ◽  
Author(s):  
Kieran Brennan ◽  
Gozie Offiah ◽  
Elaine A. McSherry ◽  
Ann M. Hopkins
Keyword(s):  
Breast Cancer ◽  
Cell Adhesion ◽  
Epithelial Cells ◽  
Cell Fate ◽  
Cancer Progression ◽  
Protein Composition ◽  
Normal Structure ◽  
Breast Cancer Progression ◽  
And Function ◽  
Cell Cell

Breast cancer is a complex and heterogeneous disease that arises from epithelial cells lining the breast ducts and lobules. Correct adhesion between adjacent epithelial cells is important in determining the normal structure and function of epithelial tissues, and there is accumulating evidence that dysregulated cell-cell adhesion is associated with many cancers. This review will focus on one cell-cell adhesion complex, the tight junction (TJ), and summarize recent evidence that TJs may participate in breast cancer development or progression. We will first outline the protein composition of TJs and discuss the functions of the TJ complex. Secondly we will examine how alterations in these functions might facilitate breast cancer initiation or progression; by focussing on the regulatory influence of TJs on cell polarity, cell fate and cell migration. Finally we will outline how pharmacological targeting of TJ proteins may be useful in limiting breast cancer progression. Overall we hope to illustrate that the relationship between TJ alterations and breast cancer is a complex one; but that this area offers promise in uncovering fundamental mechanisms linked to breast cancer progression.

scholarly journals Simultaneous knockdown of uPA and MMP9 can reduce breast cancer progression by increasing cell-cell adhesion and modulating EMT genes

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Anuradha Moirangthem ◽  
Banashree Bondhopadhyay ◽  
Mala Mukherjee ◽  
Arghya Bandyopadhyay ◽  
Narendranath Mukherjee ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Adhesion ◽  
Cancer Progression ◽  
Breast Cancer Progression ◽  
Cell Cell

scholarly journals Early Dysregulation of Cell Adhesion and Extracellular Matrix Pathways in Breast Cancer Progression

2009 ◽  
Vol 175 (3) ◽  
pp. 1292-1302 ◽  
Author(s):  
Lyndsey A. Emery ◽  
Anusri Tripathi ◽  
Chialin King ◽  
Maureen Kavanah ◽  
Jane Mendez ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Extracellular Matrix ◽  
Cell Adhesion ◽  
Cancer Progression ◽  
Breast Cancer Progression

scholarly journals KSA Antigen Ep-CAM Mediates Cell–Cell Adhesion of Pancreatic Epithelial Cells: Morphoregulatory Roles in Pancreatic Islet Development

1998 ◽  
Vol 140 (6) ◽  
pp. 1519-1534 ◽  
Author(s):  
V. Cirulli ◽  
L. Crisa ◽  
G.M. Beattie ◽  
M.I. Mally ◽  
A.D. Lopez ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Cell Growth ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Fate ◽  
Pancreatic Islet ◽  
Pancreatic Cell ◽  
Cell Clusters ◽  
Endocrine Differentiation ◽  
Cell Cell

Cell adhesion molecules (CAMs) are important mediators of cell–cell interactions and regulate cell fate determination by influencing growth, differentiation, and organization within tissues. The human pancarcinoma antigen KSA is a glycoprotein of 40 kD originally identified as a marker of rapidly proliferating tumors of epithelial origin. Interestingly, most normal epithelia also express this antigen, although at lower levels, suggesting that a dynamic regulation of KSA may occur during cell growth and differentiation. Recently, evidence has been provided that this glycoprotein may function as an epithelial cell adhesion molecule (Ep-CAM). Here, we report that Ep-CAM exhibits the features of a morphoregulatory molecule involved in the development of human pancreatic islets. We demonstrate that Ep-CAM expression is targeted to the lateral domain of epithelial cells of the human fetal pancreas, and that it mediates calcium-independent cell–cell adhesion. Quantitative confocal immunofluorescence in fetal pancreata identified the highest levels of Ep-CAM expression in developing islet-like cell clusters budding from the ductal epithelium, a cell compartment thought to comprise endocrine progenitors. A surprisingly reversed pattern was observed in the human adult pancreas, displaying low levels of Ep-CAM in islet cells and high levels in ducts. We further demonstrate that culture conditions promoting epithelial cell growth induce upregulation of Ep-CAM, whereas endocrine differentiation of fetal pancreatic epithelial cells, transplanted in nude mice, is associated with a downregulation of Ep-CAM expression. In addition, a blockade of Ep-CAM function by KS1/4 mAb induced insulin and glucagon gene transcription and translation in fetal pancreatic cell clusters. These results indicate that developmentally regulated expression and function of Ep-CAM play a morphoregulatory role in pancreatic islet ontogeny.

scholarly journals Oncogenic and Tumor Suppressive Components of the Cell Cycle in Breast Cancer Progression and Prognosis

Pharmaceutics ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 569
Author(s):  
Dharambir Kashyap ◽  
Vivek Kumar Garg ◽  
Elise N. Sandberg ◽  
Neelam Goel ◽  
Anupam Bishayee
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Epithelial Cells ◽  
Cancer Progression ◽  
Genetic Alterations ◽  
Breast Cancer Progression ◽  
Cyclin Dependent Kinase ◽  
Breast Epithelial Cells ◽  
Breast Epithelial ◽  
Cell Cycle Machinery

Cancer, a disease of inappropriate cell proliferation, is strongly interconnected with the cell cycle. All cancers consist of an abnormal accumulation of neoplastic cells, which are propagated toward uncontrolled cell division and proliferation in response to mitogenic signals. Mitogenic stimuli include genetic and epigenetic changes in cell cycle regulatory genes and other genes which regulate the cell cycle. This suggests that multiple, distinct pathways of genetic alterations lead to cancer development. Products of both oncogenes (including cyclin-dependent kinase (CDKs) and cyclins) and tumor suppressor genes (including cyclin-dependent kinase inhibitors) regulate cell cycle machinery and promote or suppress cell cycle progression, respectively. The identification of cyclins and CDKs help to explain and understand the molecular mechanisms of cell cycle machinery. During breast cancer tumorigenesis, cyclins A, B, C, D1, and E; cyclin-dependent kinase (CDKs); and CDK-inhibitor proteins p16, p21, p27, and p53 are known to play significant roles in cell cycle control and are tightly regulated in normal breast epithelial cells. Following mitogenic stimuli, these components are deregulated, which promotes neoplastic transformation of breast epithelial cells. Multiple studies implicate the roles of both types of components—oncogenic CDKs and cyclins, along with tumor-suppressing cyclin-dependent inhibitors—in breast cancer initiation and progression. Numerous clinical studies have confirmed that there is a prognostic significance for screening for these described components, regarding patient outcomes and their responses to therapy. The aim of this review article is to summarize the roles of oncogenic and tumor-suppressive components of the cell cycle in breast cancer progression and prognosis.

scholarly journals GATA3 targets semaphorin 3B in mammary epithelial cells to suppress breast cancer progression and metastasis

Oncogene ◽  
2017 ◽  
Vol 36 (40) ◽  
pp. 5567-5575 ◽  
Author(s):  
P Shahi ◽  
C-Y Wang ◽  
J Chou ◽  
C Hagerling ◽  
H Gonzalez Velozo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Epithelial Cells ◽  
Cancer Progression ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Breast Cancer Progression
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