Claudin-4 overexpression in epithelial ovarian cancer is associated with hypomethylation and is a potential target for modulation of tight junction barrier function using a C-terminal fragment of Clostridium perfringens enterotoxin.

Claudin-4 overexpression in epithelial ovarian cancer is associated with hypomethylation and is a potential target for modulation of tight junction barrier function using a C-terminal fragment of Clostridium perfringens enterotoxin. Research Abstract Details 

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Claudin-4 overexpression in epithelial ovarian cancer is associated with hypomethylation and is a potential target for modulation of tight junction barrier function using a C-terminal fragment of Clostridium perfringens enterotoxin. Abstract Text:

Babak Litkouhi,Joseph Kwong,Chun-Min Lo,James G Smedley,Bruce A McClane,Margarita Aponte,Zhijian Gao,Jennifer L Sarno,Jennifer Hinners,William R Welch,Ross S Berkowitz,Samuel C Mok,Elizabeth I O Garner,

BACKGROUND: Claudin-4, a tight junction (TJ) protein and receptor for the C-terminal fragment of Clostridium perfringens enterotoxin (C-CPE), is overexpressed in epithelial ovarian cancer (EOC). Previous research suggests DNA methylation is a mechanism for claudin-4 overexpression in cancer and that C-CPE acts as an absorption-enhancing agent in claudin-4-expressing cells. We sought to correlate claudin-4 overexpression in EOC with clinical outcomes and TJ barrier function, investigate DNA methylation as a mechanism for overexpression, and evaluate the effect of C-CPE on the TJ. METHODS: Claudin-4 expression in EOC was quantified and correlated with clinical outcomes. Claudin-4 methylation status was determined, and claudin-4-negative cell lines were treated with a demethylating agent. Electric cell-substrate impedance sensing was used to calculate junctional (paracellular) resistance (Rb) in EOC cells after claudin-4 silencing and after C-CPE treatment. RESULTS: Claudin-4 overexpression in EOC does not correlate with survival or other clinical endpoints and is associated with hypomethylation. Claudin-4 overexpression correlates with Rb and C-CPE treatment of EOC cells significantly decreased Rb in a dose- and claudin-4-dependent noncytotoxic manner. CONCLUSIONS: C-CPE treatment of EOC cells leads to altered TJ function. Further research is needed to determine the potential clinical applications of C-CPE in EOC drug delivery strategies.

Claudin-4 overexpression in epithelial ovarian cancer is associated with hypomethylation and is a potential target for modulation of tight junction barrier function using a C-terminal fragment of Clostridium perfringens enterotoxin. Publishing Authors By Initials

B Litkouhi,J Kwong,CM Lo,JG Smedley,BA McClane,M Aponte,Z Gao,JL Sarno,J Hinners,WR Welch,RS Berkowitz,SC Mok,EI Garner,

For similar cells: cellular structures: cell membrane: cell membrane structures: intercellular junctions: tight junctions research abstracts see: cells: cellular structures: cell membrane: cell membrane structures: intercellular junctions: tight junctions research

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Claudin-4 overexpression in epithelial ovarian cancer is associated with hypomethylation and is a potential target for modulation of tight junction barrier function using a C-terminal fragment of Clostridium perfringens enterotoxin. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Neoplasia (New York, N.Y.)

VOLUME: 9

Page Numbers: 304-14

Journal Abbreviation:

ISSN: 1476-5586

DAY: 3

MONTH: Apr

YEAR: 2007

Claudin-4 overexpression in epithelial ovarian cancer is associated with hypomethylation and is a potential target for modulation of tight junction barrier function using a C-terminal fragment of Clostridium perfringens enterotoxin. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100886622

Claudin-4 overexpression in epithelial ovarian cancer is associated with hypomethylation and is a potential target for modulation of tight junction barrier function using a C-terminal fragment of Clostridium perfringens enterotoxin. Keywords Mesh Terms:

KEYWORDS: Tight Junctions

MESH TERMS: physiology

Chemical & Substance for Abstract: Claudin-4 overexpression in epithelial ovarian cancer is associated with hypomethylation and is a potential target for modulation of tight junction barrier function using a C-terminal fragment of Clostridium perfringens enterotoxin. Information

Substance Name: enterotoxin, Clostridium

Registry Number: 0

Grant and Affiliation Information for Claudin-4 overexpression in epithelial ovarian cancer is associated with hypomethylation and is a potential target for modulation of tight junction barrier function using a C-terminal fragment of Clostridium perfringens enterotoxin.

AFFILIATION: Department of Obstetrics, Gynecology and Reproductive Biology, Division of Gynecologic Oncology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. blitkouhi@partners.org

Country: Canada

AGENCY: United States NIAID

GRANT: R37AI19844

ACRONYM: AI

MEDLINETA: Neoplasia

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