Invited Commentary: Role of Estrogen Receptor-α in Regulating Claudin-6 Expression in Breast Cancer Cells

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Invited Commentary: Role of Estrogen Receptor-α in Regulating Claudin-6 Expression in Breast Cancer Cells

Korean Breast Cancer Society
DOI: 10.4048/jbc.2011.14.1.76
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© 2011 Korean Breast Cancer Society | pISSN 1738-6756 eISSN 2092-9900 Tight junctions (TJs) contribute to the paracellular barrier, which is a fence that divides plasma membranes and signal transduction, acting as a multifunctional complex in vertebrate epithelial and endothelial cells [1]. The morphological features of TJs fits well with their functions. The TJ core is a fibril-like proteinaceous structure within the lipid bilayer, the so-called TJ strands [2]. Identification and characterization of TJs-asso- ciated proteins during the last two decades has unveiled the nature of TJ strands and how they are spatially organized. The interplay between integral membrane proteins, claudins, and cytoplasmic plaque proteins, ZO-1/ZO-2, is critical for TJ for- mation and function [3]. Among the TJ-associated proteins, the claudin family of membrane proteins, identified in 1998 by the Tsukita group, are key molecules in the architecture and barrier function of TJs [4]. Claudins maintain cell polarity and are involved in re- cruiting signaling proteins. Claudins are also hypothesized to be involved in the regulation of proliferation, differentiation, and other cellular functions [5]. TJ dysfunction has been presumed as a mechanism for the loss of cell adhesion and an important step in the progression of cancer to metastasis. Because claudin expression patterns are tissue- and cell-specific, recent studies have suggested that claudins might be useful molecular markers for many differ- ent cancers [6,7]. Moreover, claudins are a potential target for novel antibody-based therapies of diverse cancers [8]. Until now, 24 members of the claudin family have been iden- tified. The role of claudins in breast cancer is unknown and not well-explored, but recent reports have shown that claudins 3 and 4 are overexpressed in breast cancer, whereas claudins 1 and 7 are downregulated or completely absent [9-11]. Further- more, Szasz et al. [12] indicated that the loss

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