Title
Possible angiogenic roles for claudin-4 in ovarian cancer
Abbreviated Journal Title
Cancer Biol. Ther.
Keywords
ovarian cancer; expression profiling; claudin; interleukin; interferon; angiogenesis; SURFACE EPITHELIAL-CELLS; DIFFERENTIAL GENE-EXPRESSION; ENDOTHELIAL; GROWTH-FACTOR; TIGHT JUNCTION PROTEINS; HUMAN-MELANOMA; MATRIX; METALLOPROTEINASES; INHIBIT ANGIOGENESIS; REDUCED EXPRESSION; SEROUS; PAPILLARY; TUMOR-GROWTH; Oncology
Abstract
Claudin proteins are frequently overexpressed in various tumors such as breast, prostate and ovarian cancer. While their functions in cancer have not been completely elucidated, roles in survival, adhesion and invasion have been suggested. In order to clarify the roles of claudins in ovarian cancer, we have performed gene expression profiling of ovarian surface epithelial cells overexpressing claudin-4 and compared the expression patterns to the parental, non-expressing cells. Claudin-4 expression leads to the differential expression of several genes, including many that have previously been implicated in angiogenesis. In particular, angiogenic cytokines, such as IL-8, were found elevated while genes of the angiostatic interferon pathway were found downregulated. In vitro assays show that claudin-4-expressing cells produce factors that can stimulate angiogenesis as measured by tube formation and migration in HUVEC cells. In addition, an in vivo mouse dorsal skinfold assay confirms that cells expressing claudin-4 secrete factors that can mediate angiogenesis in the dorsal skin of mice. Our data suggest a novel function for claudin-4 in cancer and provide an additional rationale for its common overexpression in human tumors.
Journal Title
Cancer Biology & Therapy
Volume
8
Issue/Number
19
Publication Date
1-1-2009
Document Type
Article
Language
English
First Page
1806
Last Page
1814
WOS Identifier
ISSN
1538-4047
Recommended Citation
"Possible angiogenic roles for claudin-4 in ovarian cancer" (2009). Faculty Bibliography 2000s. 1790.
https://stars.library.ucf.edu/facultybib2000/1790