期刊
ONCOLOGY LETTERS
卷 10, 期 1, 页码 156-162出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/ol.2015.3160
关键词
cell motility; tight junctions; metastasis
类别
资金
- National Science Foundation Major Research Instrumentation Grant [0922258]
- Joe and Jessie Crump Fund at JP Morgan Bank
- ACS Andrew W. Mellon Integrated Scholarly Grant through the Undergraduate Science Education Program [52007558]
- Howard Hughes Medical Institute through the Undergraduate Science Education Program [52007558]
- Southwestern University Faculty-Student Collaborative Projects fund
- Div Of Biological Infrastructure
- Direct For Biological Sciences [0922258] Funding Source: National Science Foundation
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.
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