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Finally, we transfected HeLa-siCIIA1 Amprenavir either with an siRNA duplex for claudin-1 (siCLDN1) [15] or with a control siRNA for GFP (siCON) and then examined cell migration and invasion. Immunoblot analysis confirmed that the abundance of endogenous claudin-1 was greatly reduced in HeLa-siCIIA1 cells transfected with siCLDN1 compared with that in the cells transfected with siCON (Fig. 4C). Depletion of claudin-1 by RNAi reversed the inhibitory effects of CIIA siRNA on HeLa cell migration and invasion (Fig. 4D and E). Together, these results suggest that CIIA promotes cell migration and invasion, and that these effects are mediated, at least in part, through down-regulation of claudin-1.
Tight-junctions determine epithelial cell polarity by forming a barrier between the apical and basolateral domains of the plasma membrane. Many cancer cells thus exhibit loss of tight-junction integrity as well as disruption of cell polarity. Together with occludin, claudins constitute the backbone of tight-junction strands [16]. The expression of claudin-1 has been shown to be reduced in breast cancer cells [17] and [18] and colon cancer [19]. Our data now indicate that depletion of claudin-1 promotes cell migration and invasion, revealing a potentially important role for claudin-1 in the invasiveness of epithelial cells.