Expression of Clostridium perfringens enterotoxin receptors claudin-3 and claudin-4 in prostate cancer epithelium

The mRNA for Rvp.1 (rat ventral prostate) increases in abundance before gland involution after androgen deprivation. Rvp.1 is homologous to CPE-R, the high-affinity intestinal epithelial receptor for Clostridium perfringens enterotoxin (CPE), and is sufficient to mediate CPE binding and trigger subs...

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Veröffentlicht in:Cancer research (Chicago, Ill.) Ill.), 2001-11, Vol.61 (21), p.7878-7881
Hauptverfasser: HAIYAN LONG, CREAN, Colin D, LEE, Wei-Hua, CUMMINGS, O. William, GABIG, Theodore G
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container_issue 21
container_start_page 7878
container_title Cancer research (Chicago, Ill.)
container_volume 61
creator HAIYAN LONG
CREAN, Colin D
LEE, Wei-Hua
CUMMINGS, O. William
GABIG, Theodore G
description The mRNA for Rvp.1 (rat ventral prostate) increases in abundance before gland involution after androgen deprivation. Rvp.1 is homologous to CPE-R, the high-affinity intestinal epithelial receptor for Clostridium perfringens enterotoxin (CPE), and is sufficient to mediate CPE binding and trigger subsequent toxin-mediated cytolysis. Rvp.1 (claudin-3) and CPE-R (claudin-4) are members of a larger family of transmembrane tissue-specific claudin proteins that are essential components of intercellular tight junction structures regulating paracellular ion flux. However, claudin-3 and claudin-4 are the only family members capable of mediating CPE binding and cytolysis. The present study was designed to study the expression of claudin-3 and claudin-4 in human prostate tissue as potential targets for CPE toxin-mediated therapy for prostate cancer. On human multiple-tissue Northern blot analysis, mRNAs for both claudin-3 and claudin-4 were expressed at high levels in prostate tissue. In normal prostate tissue, expression of claudin-3 was localized exclusively within acinar epithelial cells by in situ mRNA hybridization. Compared with expression within prostate epithelial cells in surrounding normal glandular tissue, expression of claudin-3 mRNA remained high in the epithelium of prostate adenocarcinoma (10 of 10) and prostatic intraepithelial neoplasia (five of five). Prostate adenocarcinoma cells metastatic to bone were obtained from a patient with disease progression during antiandrogen therapy. These metastatic cells were prostate-specific antigen-positive by immunohistochemical staining and also expressed functional CPE receptors as measured by sensitivity to CPE-induced cell lysis. The persistent high level of claudin-3 expression in prostate adenocarcinoma and functional cytotoxicity of CPE in metastatic androgen-independent prostate adenocarcinoma suggests a new potential therapeutic strategy for prostate cancer.
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William ; GABIG, Theodore G</creator><creatorcontrib>HAIYAN LONG ; CREAN, Colin D ; LEE, Wei-Hua ; CUMMINGS, O. William ; GABIG, Theodore G</creatorcontrib><description>The mRNA for Rvp.1 (rat ventral prostate) increases in abundance before gland involution after androgen deprivation. Rvp.1 is homologous to CPE-R, the high-affinity intestinal epithelial receptor for Clostridium perfringens enterotoxin (CPE), and is sufficient to mediate CPE binding and trigger subsequent toxin-mediated cytolysis. Rvp.1 (claudin-3) and CPE-R (claudin-4) are members of a larger family of transmembrane tissue-specific claudin proteins that are essential components of intercellular tight junction structures regulating paracellular ion flux. However, claudin-3 and claudin-4 are the only family members capable of mediating CPE binding and cytolysis. The present study was designed to study the expression of claudin-3 and claudin-4 in human prostate tissue as potential targets for CPE toxin-mediated therapy for prostate cancer. On human multiple-tissue Northern blot analysis, mRNAs for both claudin-3 and claudin-4 were expressed at high levels in prostate tissue. In normal prostate tissue, expression of claudin-3 was localized exclusively within acinar epithelial cells by in situ mRNA hybridization. Compared with expression within prostate epithelial cells in surrounding normal glandular tissue, expression of claudin-3 mRNA remained high in the epithelium of prostate adenocarcinoma (10 of 10) and prostatic intraepithelial neoplasia (five of five). Prostate adenocarcinoma cells metastatic to bone were obtained from a patient with disease progression during antiandrogen therapy. These metastatic cells were prostate-specific antigen-positive by immunohistochemical staining and also expressed functional CPE receptors as measured by sensitivity to CPE-induced cell lysis. The persistent high level of claudin-3 expression in prostate adenocarcinoma and functional cytotoxicity of CPE in metastatic androgen-independent prostate adenocarcinoma suggests a new potential therapeutic strategy for prostate cancer.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>PMID: 11691807</identifier><identifier>CODEN: CNREA8</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Adenocarcinoma - drug therapy ; Adenocarcinoma - metabolism ; Adenocarcinoma - secondary ; Androgens - physiology ; Animals ; Biological and medical sciences ; Bone Marrow Neoplasms - drug therapy ; Bone Marrow Neoplasms - metabolism ; Bone Marrow Neoplasms - secondary ; Cercopithecus aethiops ; Claudin-3 ; Claudin-4 ; Clostridium perfringens - genetics ; Clostridium perfringens - metabolism ; Enterotoxins - metabolism ; Enterotoxins - toxicity ; Epithelial Cells - metabolism ; Epithelial Cells - pathology ; Humans ; Male ; Medical sciences ; Membrane Proteins - biosynthesis ; Membrane Proteins - genetics ; Neoplasms, Hormone-Dependent - drug therapy ; Neoplasms, Hormone-Dependent - metabolism ; Nephrology. Urinary tract diseases ; Prostatic Neoplasms - drug therapy ; Prostatic Neoplasms - metabolism ; RNA, Messenger - biosynthesis ; RNA, Messenger - genetics ; Tumors of the urinary system ; Urinary tract. 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William</creatorcontrib><creatorcontrib>GABIG, Theodore G</creatorcontrib><title>Expression of Clostridium perfringens enterotoxin receptors claudin-3 and claudin-4 in prostate cancer epithelium</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>The mRNA for Rvp.1 (rat ventral prostate) increases in abundance before gland involution after androgen deprivation. Rvp.1 is homologous to CPE-R, the high-affinity intestinal epithelial receptor for Clostridium perfringens enterotoxin (CPE), and is sufficient to mediate CPE binding and trigger subsequent toxin-mediated cytolysis. Rvp.1 (claudin-3) and CPE-R (claudin-4) are members of a larger family of transmembrane tissue-specific claudin proteins that are essential components of intercellular tight junction structures regulating paracellular ion flux. However, claudin-3 and claudin-4 are the only family members capable of mediating CPE binding and cytolysis. The present study was designed to study the expression of claudin-3 and claudin-4 in human prostate tissue as potential targets for CPE toxin-mediated therapy for prostate cancer. On human multiple-tissue Northern blot analysis, mRNAs for both claudin-3 and claudin-4 were expressed at high levels in prostate tissue. In normal prostate tissue, expression of claudin-3 was localized exclusively within acinar epithelial cells by in situ mRNA hybridization. Compared with expression within prostate epithelial cells in surrounding normal glandular tissue, expression of claudin-3 mRNA remained high in the epithelium of prostate adenocarcinoma (10 of 10) and prostatic intraepithelial neoplasia (five of five). Prostate adenocarcinoma cells metastatic to bone were obtained from a patient with disease progression during antiandrogen therapy. These metastatic cells were prostate-specific antigen-positive by immunohistochemical staining and also expressed functional CPE receptors as measured by sensitivity to CPE-induced cell lysis. The persistent high level of claudin-3 expression in prostate adenocarcinoma and functional cytotoxicity of CPE in metastatic androgen-independent prostate adenocarcinoma suggests a new potential therapeutic strategy for prostate cancer.</description><subject>Adenocarcinoma - drug therapy</subject><subject>Adenocarcinoma - metabolism</subject><subject>Adenocarcinoma - secondary</subject><subject>Androgens - physiology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Bone Marrow Neoplasms - drug therapy</subject><subject>Bone Marrow Neoplasms - metabolism</subject><subject>Bone Marrow Neoplasms - secondary</subject><subject>Cercopithecus aethiops</subject><subject>Claudin-3</subject><subject>Claudin-4</subject><subject>Clostridium perfringens - genetics</subject><subject>Clostridium perfringens - metabolism</subject><subject>Enterotoxins - metabolism</subject><subject>Enterotoxins - toxicity</subject><subject>Epithelial Cells - metabolism</subject><subject>Epithelial Cells - pathology</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Proteins - biosynthesis</subject><subject>Membrane Proteins - genetics</subject><subject>Neoplasms, Hormone-Dependent - drug therapy</subject><subject>Neoplasms, Hormone-Dependent - metabolism</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Prostatic Neoplasms - drug therapy</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>RNA, Messenger - biosynthesis</subject><subject>RNA, Messenger - genetics</subject><subject>Tumors of the urinary system</subject><subject>Urinary tract. 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William ; GABIG, Theodore G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h271t-be219bc17869dbe7122139ba03dd18a151d798aedde9d63f49fe67619aa2fd933</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Adenocarcinoma - drug therapy</topic><topic>Adenocarcinoma - metabolism</topic><topic>Adenocarcinoma - secondary</topic><topic>Androgens - physiology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Bone Marrow Neoplasms - drug therapy</topic><topic>Bone Marrow Neoplasms - metabolism</topic><topic>Bone Marrow Neoplasms - secondary</topic><topic>Cercopithecus aethiops</topic><topic>Claudin-3</topic><topic>Claudin-4</topic><topic>Clostridium perfringens - genetics</topic><topic>Clostridium perfringens - metabolism</topic><topic>Enterotoxins - metabolism</topic><topic>Enterotoxins - toxicity</topic><topic>Epithelial Cells - metabolism</topic><topic>Epithelial Cells - pathology</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane Proteins - biosynthesis</topic><topic>Membrane Proteins - genetics</topic><topic>Neoplasms, Hormone-Dependent - drug therapy</topic><topic>Neoplasms, Hormone-Dependent - metabolism</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Prostatic Neoplasms - drug therapy</topic><topic>Prostatic Neoplasms - metabolism</topic><topic>RNA, Messenger - biosynthesis</topic><topic>RNA, Messenger - genetics</topic><topic>Tumors of the urinary system</topic><topic>Urinary tract. Prostate gland</topic><topic>Vero Cells</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>HAIYAN LONG</creatorcontrib><creatorcontrib>CREAN, Colin D</creatorcontrib><creatorcontrib>LEE, Wei-Hua</creatorcontrib><creatorcontrib>CUMMINGS, O. William</creatorcontrib><creatorcontrib>GABIG, Theodore G</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Cancer research (Chicago, Ill.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>HAIYAN LONG</au><au>CREAN, Colin D</au><au>LEE, Wei-Hua</au><au>CUMMINGS, O. William</au><au>GABIG, Theodore G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression of Clostridium perfringens enterotoxin receptors claudin-3 and claudin-4 in prostate cancer epithelium</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>2001-11-01</date><risdate>2001</risdate><volume>61</volume><issue>21</issue><spage>7878</spage><epage>7881</epage><pages>7878-7881</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><coden>CNREA8</coden><abstract>The mRNA for Rvp.1 (rat ventral prostate) increases in abundance before gland involution after androgen deprivation. Rvp.1 is homologous to CPE-R, the high-affinity intestinal epithelial receptor for Clostridium perfringens enterotoxin (CPE), and is sufficient to mediate CPE binding and trigger subsequent toxin-mediated cytolysis. Rvp.1 (claudin-3) and CPE-R (claudin-4) are members of a larger family of transmembrane tissue-specific claudin proteins that are essential components of intercellular tight junction structures regulating paracellular ion flux. However, claudin-3 and claudin-4 are the only family members capable of mediating CPE binding and cytolysis. The present study was designed to study the expression of claudin-3 and claudin-4 in human prostate tissue as potential targets for CPE toxin-mediated therapy for prostate cancer. On human multiple-tissue Northern blot analysis, mRNAs for both claudin-3 and claudin-4 were expressed at high levels in prostate tissue. In normal prostate tissue, expression of claudin-3 was localized exclusively within acinar epithelial cells by in situ mRNA hybridization. Compared with expression within prostate epithelial cells in surrounding normal glandular tissue, expression of claudin-3 mRNA remained high in the epithelium of prostate adenocarcinoma (10 of 10) and prostatic intraepithelial neoplasia (five of five). Prostate adenocarcinoma cells metastatic to bone were obtained from a patient with disease progression during antiandrogen therapy. These metastatic cells were prostate-specific antigen-positive by immunohistochemical staining and also expressed functional CPE receptors as measured by sensitivity to CPE-induced cell lysis. The persistent high level of claudin-3 expression in prostate adenocarcinoma and functional cytotoxicity of CPE in metastatic androgen-independent prostate adenocarcinoma suggests a new potential therapeutic strategy for prostate cancer.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>11691807</pmid><tpages>4</tpages></addata></record>
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ispartof Cancer research (Chicago, Ill.), 2001-11, Vol.61 (21), p.7878-7881
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source MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; American Association for Cancer Research
subjects Adenocarcinoma - drug therapy
Adenocarcinoma - metabolism
Adenocarcinoma - secondary
Androgens - physiology
Animals
Biological and medical sciences
Bone Marrow Neoplasms - drug therapy
Bone Marrow Neoplasms - metabolism
Bone Marrow Neoplasms - secondary
Cercopithecus aethiops
Claudin-3
Claudin-4
Clostridium perfringens - genetics
Clostridium perfringens - metabolism
Enterotoxins - metabolism
Enterotoxins - toxicity
Epithelial Cells - metabolism
Epithelial Cells - pathology
Humans
Male
Medical sciences
Membrane Proteins - biosynthesis
Membrane Proteins - genetics
Neoplasms, Hormone-Dependent - drug therapy
Neoplasms, Hormone-Dependent - metabolism
Nephrology. Urinary tract diseases
Prostatic Neoplasms - drug therapy
Prostatic Neoplasms - metabolism
RNA, Messenger - biosynthesis
RNA, Messenger - genetics
Tumors of the urinary system
Urinary tract. Prostate gland
Vero Cells
title Expression of Clostridium perfringens enterotoxin receptors claudin-3 and claudin-4 in prostate cancer epithelium
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