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• W1968272227 abstract "Cancer cells often exhibit loss of functional tight junctions (TJ), and disruption of the TJ structure is associated with cancer development. However, whether loss of a certain type of claudin, an integral membrane protein of TJ, is involved in malignant phenotypes remains to be clarified. Based on a report that claudin-6 functions as a tumor suppressor for breast cancer, the authors show here that suppression of claudin-6 expression results in increased resistance to various apoptogens, and causally enhances anchorage-independent growth properties. Because claudin-6 expression is partially silenced by promoter CpG island hypermethylation in MCF7 breast carcinoma cells, a synergistic effect of a demethylator and histone deacetylase inhibitor up-regulates the expression of endogenous claudin-6, which is sufficient for apoptotic sensitization and abrogation of colony-forming efficacy. In addition, decreased expression of claudin-6 promotes cellular invasiveness and transendothelial migration, accompanied by an increase in matrix metalloproteinase activity. These data suggest that the methylator phenotype of claudin-6 may at least partially contribute to enhanced tumorigenic and invasive properties of breast carcinoma cells." @default.
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• W1968272227 date "2007-07-23" @default.
• W1968272227 modified "2023-10-15" @default.
• W1968272227 title "Epigenetic silencing of claudin-6 promotes anchorage-independent growth of breast carcinoma cells" @default.
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• W1968272227 doi "https://doi.org/10.1111/j.1349-7006.2007.00569.x" @default.
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