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Review
. 2010:2010:460607.
doi: 10.1155/2010/460607. Epub 2009 Nov 15.

Tight junctions: a barrier to the initiation and progression of breast cancer?

Kieran Brennan  1 , Gozie Offiah, Elaine A McSherry, Ann M Hopkins
Affiliations
Review

Tight junctions: a barrier to the initiation and progression of breast cancer?

Kieran Brennan et al. J Biomed Biotechnol. 2010.

Abstract

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.

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Figures

Figure 1
Figure 1
Epithelial cell-cell adhesion complexes.
Figure 2
Figure 2
The potential influence of TJ proteins on breast cancer development. Breast cancer predominantly begins in luminal epithelial cells lining the normal breast ducts (a). Alterations in TJ proteins may lead to the initiation of breast tumourigenesis in at least two ways. Firstly, TJ alterations may favour decreased cellular apoptosis and increased proliferation leading to uncontrolled growth, such as is seen in ductal carcinoma in situ lesions (b). Secondly, TJ alterations may decrease cell adhesion and increase motility, facilitating cancer cell migration as seen during invasion and basement membrane breakdown in early primary invasive breast carcinoma (c). Breast carcinoma likely requires coordinated efforts of both increased proliferation and increased motility to progress to metastatic stages (d).
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