Epidermal growth factor modulates claudins and tight junctional functions in ovarian cancer cell lines
Ovarian adenocarcinomas, like human ovarian surface epithelial cells, form functional tight junctions. Tight junction molecules claudin-3 and claudin-4, which are the receptors of Clostridium perfringens enterotoxin (CPE), are abnormally upregulated in epithelial ovarian cancers of all subtypes incl...
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| Veröffentlicht in: | Histochemistry and cell biology 2012-08, Vol.138 (2), p.323-338 |
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| creator | Ogawa, Marie Kojima, Takashi Someya, Masayuki Nomura, Kazuaki Takasawa, Akira Murata, Masaki Tanaka, Satoshi Saito, Tsuyoshi Sawada, Norimasa |
| description | Ovarian adenocarcinomas, like human ovarian surface epithelial cells, form functional tight junctions. Tight junction molecules claudin-3 and claudin-4, which are the receptors of
Clostridium perfringens
enterotoxin (CPE), are abnormally upregulated in epithelial ovarian cancers of all subtypes including, mucinous cystadenocarcinoma and serous cystadenocarcinoma.
Clostridium perfringens
enterotoxin may be a novel tumor-targeted therapy for ovarian cancers. In epithelial ovarian cancers, overexpression of epidermal growth factor receptor has been observed and the exogenous ligand EGF induces epithelial–mesenchymal transition in ovarian surface epithelium. Epidermal growth factor (EGF) signaling modulates expression of claudins with changes of fence and barrier functions in various cell types. However, the regulation of tight junctions by EGF in ovarian cancers remains unclear. In the present study, to investigate the mechanisms of the regulation of tight junctions in ovarian cancers, ovarian cancer cell lines mucinous cystadenocarcinoma (MCAS) and serous cystadenocarcinoma (HUOA) were treated with EGF. Epidermal growth factor downregulated claudin-3 in MCAS and claudin-4 in HUOA by inducing degradation of the proteins with changes in structures and functions of tight junctions via the MEK/ERK or PI3K/Akt signaling pathway. In addition, in HUOA but not MCAS, EGF downregulated the cytotoxic effect of CPE via claudin-4. Thus, there were different mechanisms for regulation of claudins by EGF between subtypes of epithelial ovarian cancer cells in vitro. These results indicate that EGF may affect claudins and tight junctional functions in ovarian cancer cells during cancer progression. |
| doi_str_mv | 10.1007/s00418-012-0956-x |
| format | Article |
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Clostridium perfringens
enterotoxin (CPE), are abnormally upregulated in epithelial ovarian cancers of all subtypes including, mucinous cystadenocarcinoma and serous cystadenocarcinoma.
Clostridium perfringens
enterotoxin may be a novel tumor-targeted therapy for ovarian cancers. In epithelial ovarian cancers, overexpression of epidermal growth factor receptor has been observed and the exogenous ligand EGF induces epithelial–mesenchymal transition in ovarian surface epithelium. Epidermal growth factor (EGF) signaling modulates expression of claudins with changes of fence and barrier functions in various cell types. However, the regulation of tight junctions by EGF in ovarian cancers remains unclear. In the present study, to investigate the mechanisms of the regulation of tight junctions in ovarian cancers, ovarian cancer cell lines mucinous cystadenocarcinoma (MCAS) and serous cystadenocarcinoma (HUOA) were treated with EGF. Epidermal growth factor downregulated claudin-3 in MCAS and claudin-4 in HUOA by inducing degradation of the proteins with changes in structures and functions of tight junctions via the MEK/ERK or PI3K/Akt signaling pathway. In addition, in HUOA but not MCAS, EGF downregulated the cytotoxic effect of CPE via claudin-4. Thus, there were different mechanisms for regulation of claudins by EGF between subtypes of epithelial ovarian cancer cells in vitro. These results indicate that EGF may affect claudins and tight junctional functions in ovarian cancer cells during cancer progression.</description><identifier>ISSN: 0948-6143</identifier><identifier>EISSN: 1432-119X</identifier><identifier>DOI: 10.1007/s00418-012-0956-x</identifier><identifier>PMID: 22544349</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject>Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Cell Line, Tumor ; Cellular biology ; Claudin-1 - genetics ; Claudin-1 - metabolism ; Claudin-3 - genetics ; Claudin-3 - metabolism ; Claudin-4 - genetics ; Claudin-4 - metabolism ; Claudins - genetics ; Claudins - metabolism ; Cystadenocarcinoma, Serous - genetics ; Cystadenocarcinoma, Serous - metabolism ; Developmental Biology ; Epidermal Growth Factor - metabolism ; Female ; Humans ; Original Article ; Ovarian cancer ; Ovarian Neoplasms - genetics ; Ovarian Neoplasms - metabolism ; RNA, Messenger - metabolism ; Signal transduction ; Signal Transduction - genetics ; Tight Junctions - physiology</subject><ispartof>Histochemistry and cell biology, 2012-08, Vol.138 (2), p.323-338</ispartof><rights>Springer-Verlag 2012</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c438t-4c25bc5d19d5366d3981104e5ccb707eb73f649d597b088989971db7f355323f3</citedby><cites>FETCH-LOGICAL-c438t-4c25bc5d19d5366d3981104e5ccb707eb73f649d597b088989971db7f355323f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00418-012-0956-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00418-012-0956-x$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22544349$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ogawa, Marie</creatorcontrib><creatorcontrib>Kojima, Takashi</creatorcontrib><creatorcontrib>Someya, Masayuki</creatorcontrib><creatorcontrib>Nomura, Kazuaki</creatorcontrib><creatorcontrib>Takasawa, Akira</creatorcontrib><creatorcontrib>Murata, Masaki</creatorcontrib><creatorcontrib>Tanaka, Satoshi</creatorcontrib><creatorcontrib>Saito, Tsuyoshi</creatorcontrib><creatorcontrib>Sawada, Norimasa</creatorcontrib><title>Epidermal growth factor modulates claudins and tight junctional functions in ovarian cancer cell lines</title><title>Histochemistry and cell biology</title><addtitle>Histochem Cell Biol</addtitle><addtitle>Histochem Cell Biol</addtitle><description>Ovarian adenocarcinomas, like human ovarian surface epithelial cells, form functional tight junctions. Tight junction molecules claudin-3 and claudin-4, which are the receptors of
Clostridium perfringens
enterotoxin (CPE), are abnormally upregulated in epithelial ovarian cancers of all subtypes including, mucinous cystadenocarcinoma and serous cystadenocarcinoma.
Clostridium perfringens
enterotoxin may be a novel tumor-targeted therapy for ovarian cancers. In epithelial ovarian cancers, overexpression of epidermal growth factor receptor has been observed and the exogenous ligand EGF induces epithelial–mesenchymal transition in ovarian surface epithelium. Epidermal growth factor (EGF) signaling modulates expression of claudins with changes of fence and barrier functions in various cell types. However, the regulation of tight junctions by EGF in ovarian cancers remains unclear. In the present study, to investigate the mechanisms of the regulation of tight junctions in ovarian cancers, ovarian cancer cell lines mucinous cystadenocarcinoma (MCAS) and serous cystadenocarcinoma (HUOA) were treated with EGF. Epidermal growth factor downregulated claudin-3 in MCAS and claudin-4 in HUOA by inducing degradation of the proteins with changes in structures and functions of tight junctions via the MEK/ERK or PI3K/Akt signaling pathway. In addition, in HUOA but not MCAS, EGF downregulated the cytotoxic effect of CPE via claudin-4. Thus, there were different mechanisms for regulation of claudins by EGF between subtypes of epithelial ovarian cancer cells in vitro. These results indicate that EGF may affect claudins and tight junctional functions in ovarian cancer cells during cancer progression.</description><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Cell Line, Tumor</subject><subject>Cellular biology</subject><subject>Claudin-1 - genetics</subject><subject>Claudin-1 - metabolism</subject><subject>Claudin-3 - genetics</subject><subject>Claudin-3 - metabolism</subject><subject>Claudin-4 - genetics</subject><subject>Claudin-4 - metabolism</subject><subject>Claudins - genetics</subject><subject>Claudins - metabolism</subject><subject>Cystadenocarcinoma, Serous - genetics</subject><subject>Cystadenocarcinoma, Serous - metabolism</subject><subject>Developmental Biology</subject><subject>Epidermal Growth Factor - metabolism</subject><subject>Female</subject><subject>Humans</subject><subject>Original Article</subject><subject>Ovarian cancer</subject><subject>Ovarian Neoplasms - genetics</subject><subject>Ovarian Neoplasms - metabolism</subject><subject>RNA, Messenger - metabolism</subject><subject>Signal transduction</subject><subject>Signal Transduction - genetics</subject><subject>Tight Junctions - physiology</subject><issn>0948-6143</issn><issn>1432-119X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kU9rGzEQxUVoiV0nHyCXIOgll21H_3ZXx2DSNGDoJYXcFq2ktWV2JUfabZ1vXxk7IQR60qD5vTfSPISuCHwjANX3BMBJXQChBUhRFvszNCec0YIQ-fQJzUHyuijzzQx9SWkLQISk9BzNKBWcMy7nqLvbOWPjoHq8juHvuMGd0mOIeAhm6tVoE9a9mozzCStv8OjWmxFvJ69HF3xWdacyYedx-KOiUx5r5bWNWNu-x73zNl2gz53qk708nQv0-8fd4_Jnsfp1_7C8XRWas3osuKai1cIQaQQrS8NkTQhwK7RuK6hsW7Gu5LkpqxbqWtZSVsS0VceEYJR1bIFujr67GJ4nm8ZmcOnwDOVtmFJDgAETtJIio18_oNswxfylA0WlFDVIyBQ5UjqGlKLtml10g4ovGWoOITTHEJocQnMIodlnzfXJeWoHa94Ur1vPAD0CKbf82sb3o__n-g8W5ZJ_</recordid><startdate>20120801</startdate><enddate>20120801</enddate><creator>Ogawa, Marie</creator><creator>Kojima, Takashi</creator><creator>Someya, Masayuki</creator><creator>Nomura, Kazuaki</creator><creator>Takasawa, Akira</creator><creator>Murata, Masaki</creator><creator>Tanaka, Satoshi</creator><creator>Saito, Tsuyoshi</creator><creator>Sawada, Norimasa</creator><general>Springer-Verlag</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20120801</creationdate><title>Epidermal growth factor modulates claudins and tight junctional functions in ovarian cancer cell lines</title><author>Ogawa, Marie ; Kojima, Takashi ; Someya, Masayuki ; Nomura, Kazuaki ; Takasawa, Akira ; Murata, Masaki ; Tanaka, Satoshi ; Saito, Tsuyoshi ; Sawada, Norimasa</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c438t-4c25bc5d19d5366d3981104e5ccb707eb73f649d597b088989971db7f355323f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Biology</topic><topic>Cell Line, Tumor</topic><topic>Cellular biology</topic><topic>Claudin-1 - genetics</topic><topic>Claudin-1 - metabolism</topic><topic>Claudin-3 - genetics</topic><topic>Claudin-3 - metabolism</topic><topic>Claudin-4 - genetics</topic><topic>Claudin-4 - metabolism</topic><topic>Claudins - genetics</topic><topic>Claudins - metabolism</topic><topic>Cystadenocarcinoma, Serous - genetics</topic><topic>Cystadenocarcinoma, Serous - metabolism</topic><topic>Developmental Biology</topic><topic>Epidermal Growth Factor - metabolism</topic><topic>Female</topic><topic>Humans</topic><topic>Original Article</topic><topic>Ovarian cancer</topic><topic>Ovarian Neoplasms - genetics</topic><topic>Ovarian Neoplasms - metabolism</topic><topic>RNA, Messenger - metabolism</topic><topic>Signal transduction</topic><topic>Signal Transduction - genetics</topic><topic>Tight Junctions - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ogawa, Marie</creatorcontrib><creatorcontrib>Kojima, Takashi</creatorcontrib><creatorcontrib>Someya, Masayuki</creatorcontrib><creatorcontrib>Nomura, Kazuaki</creatorcontrib><creatorcontrib>Takasawa, Akira</creatorcontrib><creatorcontrib>Murata, Masaki</creatorcontrib><creatorcontrib>Tanaka, Satoshi</creatorcontrib><creatorcontrib>Saito, Tsuyoshi</creatorcontrib><creatorcontrib>Sawada, Norimasa</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Histochemistry and cell biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ogawa, Marie</au><au>Kojima, Takashi</au><au>Someya, Masayuki</au><au>Nomura, Kazuaki</au><au>Takasawa, Akira</au><au>Murata, Masaki</au><au>Tanaka, Satoshi</au><au>Saito, Tsuyoshi</au><au>Sawada, Norimasa</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Epidermal growth factor modulates claudins and tight junctional functions in ovarian cancer cell lines</atitle><jtitle>Histochemistry and cell biology</jtitle><stitle>Histochem Cell Biol</stitle><addtitle>Histochem Cell Biol</addtitle><date>2012-08-01</date><risdate>2012</risdate><volume>138</volume><issue>2</issue><spage>323</spage><epage>338</epage><pages>323-338</pages><issn>0948-6143</issn><eissn>1432-119X</eissn><abstract>Ovarian adenocarcinomas, like human ovarian surface epithelial cells, form functional tight junctions. Tight junction molecules claudin-3 and claudin-4, which are the receptors of
Clostridium perfringens
enterotoxin (CPE), are abnormally upregulated in epithelial ovarian cancers of all subtypes including, mucinous cystadenocarcinoma and serous cystadenocarcinoma.
Clostridium perfringens
enterotoxin may be a novel tumor-targeted therapy for ovarian cancers. In epithelial ovarian cancers, overexpression of epidermal growth factor receptor has been observed and the exogenous ligand EGF induces epithelial–mesenchymal transition in ovarian surface epithelium. Epidermal growth factor (EGF) signaling modulates expression of claudins with changes of fence and barrier functions in various cell types. However, the regulation of tight junctions by EGF in ovarian cancers remains unclear. In the present study, to investigate the mechanisms of the regulation of tight junctions in ovarian cancers, ovarian cancer cell lines mucinous cystadenocarcinoma (MCAS) and serous cystadenocarcinoma (HUOA) were treated with EGF. Epidermal growth factor downregulated claudin-3 in MCAS and claudin-4 in HUOA by inducing degradation of the proteins with changes in structures and functions of tight junctions via the MEK/ERK or PI3K/Akt signaling pathway. In addition, in HUOA but not MCAS, EGF downregulated the cytotoxic effect of CPE via claudin-4. Thus, there were different mechanisms for regulation of claudins by EGF between subtypes of epithelial ovarian cancer cells in vitro. These results indicate that EGF may affect claudins and tight junctional functions in ovarian cancer cells during cancer progression.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer-Verlag</pub><pmid>22544349</pmid><doi>10.1007/s00418-012-0956-x</doi><tpages>16</tpages></addata></record> |
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| subjects | Biochemistry Biomedical and Life Sciences Biomedicine Cell Biology Cell Line, Tumor Cellular biology Claudin-1 - genetics Claudin-1 - metabolism Claudin-3 - genetics Claudin-3 - metabolism Claudin-4 - genetics Claudin-4 - metabolism Claudins - genetics Claudins - metabolism Cystadenocarcinoma, Serous - genetics Cystadenocarcinoma, Serous - metabolism Developmental Biology Epidermal Growth Factor - metabolism Female Humans Original Article Ovarian cancer Ovarian Neoplasms - genetics Ovarian Neoplasms - metabolism RNA, Messenger - metabolism Signal transduction Signal Transduction - genetics Tight Junctions - physiology |
| title | Epidermal growth factor modulates claudins and tight junctional functions in ovarian cancer cell lines |
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