Inhibition of pregnane X receptor pathway contributes to the cell growth inhibition and apoptosis of anticancer agents in ovarian cancer cells
Epithelial ovarian cancer remains the most devastating gynecologic cancer with drug resistance and rapid recurrence. Pregnane X receptor (PXR) is a nuclear receptor that affects drug metabolism/efflux and drug-drug interaction through control of multiple drug resistance 1 (MDR1), which implies a maj...
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| Veröffentlicht in: | International journal of oncology 2016-09, Vol.49 (3), p.1211-1220 |
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| container_title | International journal of oncology |
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| creator | Masuyama, Hisashi Nakamura, Keiichiro Nobumoto, Etsuko Hiramatsu, Yuji |
| description | Epithelial ovarian cancer remains the most devastating gynecologic cancer with drug resistance and rapid recurrence. Pregnane X receptor (PXR) is a nuclear receptor that affects drug metabolism/efflux and drug-drug interaction through control of multiple drug resistance 1 (MDR1), which implies a major role in multidrug resistance, and other genes. We examined whether the inhibition of PXR-mediated pathway using siRNA interference and an antagonist for PXR could influence the paclitaxel and cisplatin cytotoxicity in ovarian cancer cells. PXR agonists, phthalate and pregnenolone had significant positive effects on cytochrome P450 (CYP) 3A4 expression and PXR-mediated transcription through the CYP3A4 promoter, whereas MDR1 expression and PXR-mediated transcription though the MDR1 promoter were significantly increased in the presence of paclitaxel or cisplatin. Downregulation of PXR suppressed the augmented MDR1 expression and PXR-mediated transcription by PXR ligands, and significantly enhanced cell growth inhibition and apoptosis in the presence of paclitaxel or cisplatin. Additionally, ketoconazole, a PXR antagonist, suppressed the augmented MDR1 expression and PXR-mediated transactivation by paclitaxel and cisplatin, and enhanced cell growth inhibition and apoptosis in their presence. In conclusion, inhibition of PXR-mediated pathways could be a novel means of augmenting sensitivity, or overcoming resistance to anticancer agents for ovarian cancer. |
| doi_str_mv | 10.3892/ijo.2016.3611 |
| format | Article |
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Pregnane X receptor (PXR) is a nuclear receptor that affects drug metabolism/efflux and drug-drug interaction through control of multiple drug resistance 1 (MDR1), which implies a major role in multidrug resistance, and other genes. We examined whether the inhibition of PXR-mediated pathway using siRNA interference and an antagonist for PXR could influence the paclitaxel and cisplatin cytotoxicity in ovarian cancer cells. PXR agonists, phthalate and pregnenolone had significant positive effects on cytochrome P450 (CYP) 3A4 expression and PXR-mediated transcription through the CYP3A4 promoter, whereas MDR1 expression and PXR-mediated transcription though the MDR1 promoter were significantly increased in the presence of paclitaxel or cisplatin. Downregulation of PXR suppressed the augmented MDR1 expression and PXR-mediated transcription by PXR ligands, and significantly enhanced cell growth inhibition and apoptosis in the presence of paclitaxel or cisplatin. Additionally, ketoconazole, a PXR antagonist, suppressed the augmented MDR1 expression and PXR-mediated transactivation by paclitaxel and cisplatin, and enhanced cell growth inhibition and apoptosis in their presence. In conclusion, inhibition of PXR-mediated pathways could be a novel means of augmenting sensitivity, or overcoming resistance to anticancer agents for ovarian cancer.</description><identifier>ISSN: 1019-6439</identifier><identifier>EISSN: 1791-2423</identifier><identifier>DOI: 10.3892/ijo.2016.3611</identifier><identifier>PMID: 27572875</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Antineoplastic Agents - pharmacology ; Apoptosis ; ATP Binding Cassette Transporter, Subfamily B - genetics ; Cancer therapies ; Carcinoma, Ovarian Epithelial ; Cell cycle ; Cell growth ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Cell receptors ; Cell Survival - drug effects ; Chemotherapy ; Cisplatin ; Cisplatin - pharmacology ; Drug dosages ; Drug metabolism ; Drug resistance ; Drug therapy ; Female ; Genes ; Genetic aspects ; Humans ; Ketoconazole - pharmacology ; Ligands ; Metabolism ; multiple drug resistance 1 ; Neoplasms, Glandular and Epithelial - drug therapy ; Neoplasms, Glandular and Epithelial - genetics ; Ovarian cancer ; Ovarian Neoplasms - drug therapy ; Ovarian Neoplasms - genetics ; Paclitaxel ; Paclitaxel - pharmacology ; Patient outcomes ; Patients ; Phthalic Acids - pharmacology ; Pregnane X Receptor ; Pregnenolone - pharmacology ; Prescription drugs ; Properties ; Receptors, Steroid - agonists ; Receptors, Steroid - antagonists & inhibitors ; RNA, Small Interfering - pharmacology ; Signal Transduction - drug effects</subject><ispartof>International journal of oncology, 2016-09, Vol.49 (3), p.1211-1220</ispartof><rights>Copyright © 2016, Spandidos Publications</rights><rights>COPYRIGHT 2016 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c556t-8fda76a77642e0e247d8bf22e7d5769bca0141d2ed80be91fa66426a91559cc83</citedby><cites>FETCH-LOGICAL-c556t-8fda76a77642e0e247d8bf22e7d5769bca0141d2ed80be91fa66426a91559cc83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,5571,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27572875$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Masuyama, Hisashi</creatorcontrib><creatorcontrib>Nakamura, Keiichiro</creatorcontrib><creatorcontrib>Nobumoto, Etsuko</creatorcontrib><creatorcontrib>Hiramatsu, Yuji</creatorcontrib><title>Inhibition of pregnane X receptor pathway contributes to the cell growth inhibition and apoptosis of anticancer agents in ovarian cancer cells</title><title>International journal of oncology</title><addtitle>Int J Oncol</addtitle><description>Epithelial ovarian cancer remains the most devastating gynecologic cancer with drug resistance and rapid recurrence. Pregnane X receptor (PXR) is a nuclear receptor that affects drug metabolism/efflux and drug-drug interaction through control of multiple drug resistance 1 (MDR1), which implies a major role in multidrug resistance, and other genes. We examined whether the inhibition of PXR-mediated pathway using siRNA interference and an antagonist for PXR could influence the paclitaxel and cisplatin cytotoxicity in ovarian cancer cells. PXR agonists, phthalate and pregnenolone had significant positive effects on cytochrome P450 (CYP) 3A4 expression and PXR-mediated transcription through the CYP3A4 promoter, whereas MDR1 expression and PXR-mediated transcription though the MDR1 promoter were significantly increased in the presence of paclitaxel or cisplatin. Downregulation of PXR suppressed the augmented MDR1 expression and PXR-mediated transcription by PXR ligands, and significantly enhanced cell growth inhibition and apoptosis in the presence of paclitaxel or cisplatin. Additionally, ketoconazole, a PXR antagonist, suppressed the augmented MDR1 expression and PXR-mediated transactivation by paclitaxel and cisplatin, and enhanced cell growth inhibition and apoptosis in their presence. In conclusion, inhibition of PXR-mediated pathways could be a novel means of augmenting sensitivity, or overcoming resistance to anticancer agents for ovarian cancer.</description><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis</subject><subject>ATP Binding Cassette Transporter, Subfamily B - genetics</subject><subject>Cancer therapies</subject><subject>Carcinoma, Ovarian Epithelial</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell receptors</subject><subject>Cell Survival - drug effects</subject><subject>Chemotherapy</subject><subject>Cisplatin</subject><subject>Cisplatin - pharmacology</subject><subject>Drug dosages</subject><subject>Drug metabolism</subject><subject>Drug resistance</subject><subject>Drug therapy</subject><subject>Female</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Humans</subject><subject>Ketoconazole - pharmacology</subject><subject>Ligands</subject><subject>Metabolism</subject><subject>multiple drug resistance 1</subject><subject>Neoplasms, Glandular and Epithelial - drug therapy</subject><subject>Neoplasms, Glandular and Epithelial - genetics</subject><subject>Ovarian cancer</subject><subject>Ovarian Neoplasms - drug therapy</subject><subject>Ovarian Neoplasms - genetics</subject><subject>Paclitaxel</subject><subject>Paclitaxel - pharmacology</subject><subject>Patient outcomes</subject><subject>Patients</subject><subject>Phthalic Acids - pharmacology</subject><subject>Pregnane X Receptor</subject><subject>Pregnenolone - pharmacology</subject><subject>Prescription drugs</subject><subject>Properties</subject><subject>Receptors, Steroid - agonists</subject><subject>Receptors, Steroid - antagonists & inhibitors</subject><subject>RNA, Small Interfering - pharmacology</subject><subject>Signal Transduction - drug effects</subject><issn>1019-6439</issn><issn>1791-2423</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkc9rFDEUxwdRbK0evUpA0NOsSWaSTI6l-KNQ8KLgLbzJvNnJMpuMSdbSf8K_2Qy71hYkh4Tk8z6PvG9VvWZ003Saf3C7sOGUyU0jGXtSnTOlWc1b3jwtZ8p0LdtGn1UvUtpRyoWg7Hl1xpVQvFPivPp97SfXu-yCJ2EkS8StB4_kB4locckhkgXydAt3xAafo-sPGRPJgeQJicV5JtsYbvNE3D8R-IHAEkp1cmnVgs_OgrcYCWzR51RoEn5BdODJ6WF1pZfVsxHmhK9O-0X1_dPHb1df6puvn6-vLm9qK4TMdTcOoCQoJVuOFHmrhq4fOUc1CCV1b4Gylg0ch472qNkIspASNBNCW9s1F9Xbo3eJ4ecBUza7cIi-tDRMN7zhQjcPqC3MaJwfQ45g9y5Zc9nKRokiVYXa_Icqa8C9K0PD0ZX7RwXvHhRMCHOeUpgP6-zSY7A-gjaGlCKOZoluD_HOMGrW9E1J36zpmzX9wr85_erQ73G4p__GXYD3RyAtJSM3hHTPFFPd6po2NeNF9Qc9w7gS</recordid><startdate>20160901</startdate><enddate>20160901</enddate><creator>Masuyama, Hisashi</creator><creator>Nakamura, Keiichiro</creator><creator>Nobumoto, Etsuko</creator><creator>Hiramatsu, Yuji</creator><general>D.A. 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pharmacology</topic><topic>Apoptosis</topic><topic>ATP Binding Cassette Transporter, Subfamily B - genetics</topic><topic>Cancer therapies</topic><topic>Carcinoma, Ovarian Epithelial</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell receptors</topic><topic>Cell Survival - drug effects</topic><topic>Chemotherapy</topic><topic>Cisplatin</topic><topic>Cisplatin - pharmacology</topic><topic>Drug dosages</topic><topic>Drug metabolism</topic><topic>Drug resistance</topic><topic>Drug therapy</topic><topic>Female</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Humans</topic><topic>Ketoconazole - pharmacology</topic><topic>Ligands</topic><topic>Metabolism</topic><topic>multiple drug resistance 1</topic><topic>Neoplasms, Glandular and Epithelial - drug therapy</topic><topic>Neoplasms, Glandular and Epithelial - genetics</topic><topic>Ovarian cancer</topic><topic>Ovarian Neoplasms - drug therapy</topic><topic>Ovarian Neoplasms - genetics</topic><topic>Paclitaxel</topic><topic>Paclitaxel - pharmacology</topic><topic>Patient outcomes</topic><topic>Patients</topic><topic>Phthalic Acids - pharmacology</topic><topic>Pregnane X Receptor</topic><topic>Pregnenolone - pharmacology</topic><topic>Prescription drugs</topic><topic>Properties</topic><topic>Receptors, Steroid - agonists</topic><topic>Receptors, Steroid - antagonists & inhibitors</topic><topic>RNA, Small Interfering - pharmacology</topic><topic>Signal Transduction - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Masuyama, Hisashi</creatorcontrib><creatorcontrib>Nakamura, Keiichiro</creatorcontrib><creatorcontrib>Nobumoto, Etsuko</creatorcontrib><creatorcontrib>Hiramatsu, Yuji</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>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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><jtitle>International journal of oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Masuyama, Hisashi</au><au>Nakamura, Keiichiro</au><au>Nobumoto, Etsuko</au><au>Hiramatsu, Yuji</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of pregnane X receptor pathway contributes to the cell growth inhibition and apoptosis of anticancer agents in ovarian cancer cells</atitle><jtitle>International journal of oncology</jtitle><addtitle>Int J Oncol</addtitle><date>2016-09-01</date><risdate>2016</risdate><volume>49</volume><issue>3</issue><spage>1211</spage><epage>1220</epage><pages>1211-1220</pages><issn>1019-6439</issn><eissn>1791-2423</eissn><abstract>Epithelial ovarian cancer remains the most devastating gynecologic cancer with drug resistance and rapid recurrence. Pregnane X receptor (PXR) is a nuclear receptor that affects drug metabolism/efflux and drug-drug interaction through control of multiple drug resistance 1 (MDR1), which implies a major role in multidrug resistance, and other genes. We examined whether the inhibition of PXR-mediated pathway using siRNA interference and an antagonist for PXR could influence the paclitaxel and cisplatin cytotoxicity in ovarian cancer cells. PXR agonists, phthalate and pregnenolone had significant positive effects on cytochrome P450 (CYP) 3A4 expression and PXR-mediated transcription through the CYP3A4 promoter, whereas MDR1 expression and PXR-mediated transcription though the MDR1 promoter were significantly increased in the presence of paclitaxel or cisplatin. Downregulation of PXR suppressed the augmented MDR1 expression and PXR-mediated transcription by PXR ligands, and significantly enhanced cell growth inhibition and apoptosis in the presence of paclitaxel or cisplatin. Additionally, ketoconazole, a PXR antagonist, suppressed the augmented MDR1 expression and PXR-mediated transactivation by paclitaxel and cisplatin, and enhanced cell growth inhibition and apoptosis in their presence. In conclusion, inhibition of PXR-mediated pathways could be a novel means of augmenting sensitivity, or overcoming resistance to anticancer agents for ovarian cancer.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>27572875</pmid><doi>10.3892/ijo.2016.3611</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1019-6439 |
| ispartof | International journal of oncology, 2016-09, Vol.49 (3), p.1211-1220 |
| issn | 1019-6439 1791-2423 |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Antineoplastic Agents - pharmacology Apoptosis ATP Binding Cassette Transporter, Subfamily B - genetics Cancer therapies Carcinoma, Ovarian Epithelial Cell cycle Cell growth Cell Line, Tumor Cell Proliferation - drug effects Cell receptors Cell Survival - drug effects Chemotherapy Cisplatin Cisplatin - pharmacology Drug dosages Drug metabolism Drug resistance Drug therapy Female Genes Genetic aspects Humans Ketoconazole - pharmacology Ligands Metabolism multiple drug resistance 1 Neoplasms, Glandular and Epithelial - drug therapy Neoplasms, Glandular and Epithelial - genetics Ovarian cancer Ovarian Neoplasms - drug therapy Ovarian Neoplasms - genetics Paclitaxel Paclitaxel - pharmacology Patient outcomes Patients Phthalic Acids - pharmacology Pregnane X Receptor Pregnenolone - pharmacology Prescription drugs Properties Receptors, Steroid - agonists Receptors, Steroid - antagonists & inhibitors RNA, Small Interfering - pharmacology Signal Transduction - drug effects |
| title | Inhibition of pregnane X receptor pathway contributes to the cell growth inhibition and apoptosis of anticancer agents in ovarian cancer cells |
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