Overexpression and delocalization of claudin-3 protein in MCF-7 and MDA-MB-415 breast cancer cell lines
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- Published online on: April 28, 2015 https://doi.org/10.3892/ol.2015.3160
- Pages: 156-162
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Copyright: © Todd et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Abstract
Tumor-specific deregulated expression of claudins, integral membrane proteins found in tight junctions (TJs), has indicated a possible role for TJ disruption in cancer progression. The current study demonstrates the marked overexpression of claudin‑3 protein in two breast cancer cell lines of metastatic origin (MCF-7 and MDA-MB-415). Immunofluorescence and differential detergent fractionation analyses revealed that, although claudin‑3 was primarily localized at cell junctions, it was also detected intracellularly. Similarly, the siRNA‑mediated suppression of claudin‑3 did not considerably affect its pattern of subcellular distribution relative to mock‑transfected cells. However, there appeared to be a preferential loss of claudin‑3 signal in the cytoskeletal fraction. Wound‑healing assays were conducted to assess the effect of endogenous overexpression versus siRNA‑mediated suppression of claudin‑3 on cellular motility in MCF‑7 cells. Suppression of claudin‑3 protein levels resulted in a marked decrease in the rate of cellular motility relative to mock‑transfected cells. These findings suggest that overexpression of claudin‑3 may be important in disrupting TJ integrity and thus contribute to enhanced cellular motility, a key component of tumor progression.
