MiR-23a-mediated inhibition of topoisomerase 1 expression potentiates cell response to etoposide in human hepatocellular carcinoma
microRNAs have been shown to regulate the chemosensitivity of cancer cells. The aim of this study is to investigate the role and mechanism of mir-23a in enhancing the anti-tumor effect of topoisomerase 2A (TOP2A) poison etoposide in human hepatocellular carcinoma (HCC). The anti-tumor effect of chem...
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| Veröffentlicht in: | Molecular cancer 2013-10, Vol.12 (1), p.119-119, Article 119 |
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| creator | Wang, Ning Zhu, Meifen Tsao, Sai-Wah Man, Kwan Zhang, Zhangjin Feng, Yibin |
| description | microRNAs have been shown to regulate the chemosensitivity of cancer cells. The aim of this study is to investigate the role and mechanism of mir-23a in enhancing the anti-tumor effect of topoisomerase 2A (TOP2A) poison etoposide in human hepatocellular carcinoma (HCC).
The anti-tumor effect of chemotherapeutic agents in HCC cells were examined in vitro and in vivo xenograft model. Expression of mRNA and miRNAs were determined by quantitative real-time PCR. Protein expression was analyzed by immunoblotting.
Overexpression of mir-23a could significantly potentiate the in vitro and in vivo anti-tumor effect of etoposide; however, ectopic expression of miR-23a fails to sensitize HCC cells to 5-fluorouracil treatment, indicating the miR-23a-induced cancer cell hypersensitivity in chemotherapy is TOP2A-specific though miR-23a overexpression could not directly up-regulate TOP2A expression. Topoisomerase 1(TOP1) is down-regulated in miR-23a-overexpressed HCC cells. MiR-23a could directly bind to 3'untranslated region of TOP1 mRNA, and suppress the corresponding protein expression and inhibition of miR-23a further arguments the expression of TOP1. MiR-23a was up-regulated during DNA damage in cancer cells in line with the p53 expression. Up-regulation of p53 induces mir-23a expression, while suppression of p53 inhibits miR-23a in HCC cells.
Our study sheds light on the role of miR-23a as a potential target in regulating chemosensitivity of HCC cells. |
| doi_str_mv | 10.1186/1476-4598-12-119 |
| format | Article |
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The anti-tumor effect of chemotherapeutic agents in HCC cells were examined in vitro and in vivo xenograft model. Expression of mRNA and miRNAs were determined by quantitative real-time PCR. Protein expression was analyzed by immunoblotting.
Overexpression of mir-23a could significantly potentiate the in vitro and in vivo anti-tumor effect of etoposide; however, ectopic expression of miR-23a fails to sensitize HCC cells to 5-fluorouracil treatment, indicating the miR-23a-induced cancer cell hypersensitivity in chemotherapy is TOP2A-specific though miR-23a overexpression could not directly up-regulate TOP2A expression. Topoisomerase 1(TOP1) is down-regulated in miR-23a-overexpressed HCC cells. MiR-23a could directly bind to 3'untranslated region of TOP1 mRNA, and suppress the corresponding protein expression and inhibition of miR-23a further arguments the expression of TOP1. MiR-23a was up-regulated during DNA damage in cancer cells in line with the p53 expression. Up-regulation of p53 induces mir-23a expression, while suppression of p53 inhibits miR-23a in HCC cells.
Our study sheds light on the role of miR-23a as a potential target in regulating chemosensitivity of HCC cells.</description><identifier>ISSN: 1476-4598</identifier><identifier>EISSN: 1476-4598</identifier><identifier>DOI: 10.1186/1476-4598-12-119</identifier><identifier>PMID: 24103454</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>3' Untranslated Regions ; 5-Fluorouracil ; Analysis ; Animals ; Antigens, Neoplasm - metabolism ; Antineoplastic Agents, Phytogenic - pharmacology ; Apoptosis ; Base Sequence ; Binding Sites ; Cancer ; Cancer therapies ; Carcinoma, Hepatocellular - drug therapy ; Carcinoma, Hepatocellular - metabolism ; Carcinoma, Hepatocellular - pathology ; Care and treatment ; Cell Line, Tumor ; Chemotherapy ; Cytotoxicity ; Diagnosis ; DNA Topoisomerases, Type I - genetics ; DNA Topoisomerases, Type I - metabolism ; DNA Topoisomerases, Type II - metabolism ; DNA-Binding Proteins - antagonists & inhibitors ; DNA-Binding Proteins - metabolism ; Drug Resistance, Neoplasm ; Etoposide ; Etoposide - pharmacology ; Experiments ; Fluorouracil ; Fluorouracil - pharmacology ; Gene expression ; Gene Expression Regulation, Neoplastic ; Genetic aspects ; Health aspects ; Hepatoma ; Humans ; Liver cancer ; Liver Neoplasms, Experimental - drug therapy ; Liver Neoplasms, Experimental - metabolism ; Liver Neoplasms, Experimental - pathology ; Medicine ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; MicroRNA ; MicroRNAs - genetics ; Poly-ADP-Ribose Binding Proteins ; Regulation ; RNA Interference ; Studies ; Tumor Burden ; Tumor proteins ; Tumor Suppressor Protein p53 - metabolism ; Xenograft Model Antitumor Assays</subject><ispartof>Molecular cancer, 2013-10, Vol.12 (1), p.119-119, Article 119</ispartof><rights>COPYRIGHT 2013 BioMed Central Ltd.</rights><rights>2013 Wang et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2013 Wang et al.; licensee BioMed Central Ltd. 2013 Wang et al.; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b584t-14643e30b8572b694500eaa82f9799003a3ad97188afa254eacad93c3d0d275f3</citedby><cites>FETCH-LOGICAL-b584t-14643e30b8572b694500eaa82f9799003a3ad97188afa254eacad93c3d0d275f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3856574/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3856574/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24103454$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Ning</creatorcontrib><creatorcontrib>Zhu, Meifen</creatorcontrib><creatorcontrib>Tsao, Sai-Wah</creatorcontrib><creatorcontrib>Man, Kwan</creatorcontrib><creatorcontrib>Zhang, Zhangjin</creatorcontrib><creatorcontrib>Feng, Yibin</creatorcontrib><title>MiR-23a-mediated inhibition of topoisomerase 1 expression potentiates cell response to etoposide in human hepatocellular carcinoma</title><title>Molecular cancer</title><addtitle>Mol Cancer</addtitle><description>microRNAs have been shown to regulate the chemosensitivity of cancer cells. The aim of this study is to investigate the role and mechanism of mir-23a in enhancing the anti-tumor effect of topoisomerase 2A (TOP2A) poison etoposide in human hepatocellular carcinoma (HCC).
The anti-tumor effect of chemotherapeutic agents in HCC cells were examined in vitro and in vivo xenograft model. Expression of mRNA and miRNAs were determined by quantitative real-time PCR. Protein expression was analyzed by immunoblotting.
Overexpression of mir-23a could significantly potentiate the in vitro and in vivo anti-tumor effect of etoposide; however, ectopic expression of miR-23a fails to sensitize HCC cells to 5-fluorouracil treatment, indicating the miR-23a-induced cancer cell hypersensitivity in chemotherapy is TOP2A-specific though miR-23a overexpression could not directly up-regulate TOP2A expression. Topoisomerase 1(TOP1) is down-regulated in miR-23a-overexpressed HCC cells. MiR-23a could directly bind to 3'untranslated region of TOP1 mRNA, and suppress the corresponding protein expression and inhibition of miR-23a further arguments the expression of TOP1. MiR-23a was up-regulated during DNA damage in cancer cells in line with the p53 expression. Up-regulation of p53 induces mir-23a expression, while suppression of p53 inhibits miR-23a in HCC cells.
Our study sheds light on the role of miR-23a as a potential target in regulating chemosensitivity of HCC cells.</description><subject>3' Untranslated Regions</subject><subject>5-Fluorouracil</subject><subject>Analysis</subject><subject>Animals</subject><subject>Antigens, Neoplasm - metabolism</subject><subject>Antineoplastic Agents, Phytogenic - pharmacology</subject><subject>Apoptosis</subject><subject>Base Sequence</subject><subject>Binding Sites</subject><subject>Cancer</subject><subject>Cancer therapies</subject><subject>Carcinoma, Hepatocellular - drug therapy</subject><subject>Carcinoma, Hepatocellular - metabolism</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>Care and treatment</subject><subject>Cell Line, Tumor</subject><subject>Chemotherapy</subject><subject>Cytotoxicity</subject><subject>Diagnosis</subject><subject>DNA Topoisomerases, Type I - genetics</subject><subject>DNA Topoisomerases, Type I - metabolism</subject><subject>DNA Topoisomerases, Type II - metabolism</subject><subject>DNA-Binding Proteins - antagonists & inhibitors</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Drug Resistance, Neoplasm</subject><subject>Etoposide</subject><subject>Etoposide - pharmacology</subject><subject>Experiments</subject><subject>Fluorouracil</subject><subject>Fluorouracil - pharmacology</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Hepatoma</subject><subject>Humans</subject><subject>Liver cancer</subject><subject>Liver Neoplasms, Experimental - drug therapy</subject><subject>Liver Neoplasms, Experimental - metabolism</subject><subject>Liver Neoplasms, Experimental - pathology</subject><subject>Medicine</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>MicroRNA</subject><subject>MicroRNAs - genetics</subject><subject>Poly-ADP-Ribose Binding Proteins</subject><subject>Regulation</subject><subject>RNA Interference</subject><subject>Studies</subject><subject>Tumor Burden</subject><subject>Tumor proteins</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><subject>Xenograft Model Antitumor Assays</subject><issn>1476-4598</issn><issn>1476-4598</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</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><recordid>eNp1Uk1v1DAQjRCIlsKdE7LEpZe0dmzH8QWpWpUPqRUSgrM1SSZdV4kd7KSCK78cW1uWLioXf8y89zzzxkXxmtEzxpr6nAlVl0LqpmRVyZh-UhzvQ08fnI-KFzHeUspUo8Tz4qgSjHIhxXHx69p-KSsO5YS9hQV7Yt3Wtnax3hE_kMXP3kY_YYCIhBH8MQeMMWdnv6BbMimSDseRpMTsXYItnmAmRttj0iPbdYK04gyLz8h1hEA6CJ11foKXxbMBxoiv7veT4tv7y6-bj-XV5w-fNhdXZSsbsZRM1IIjp20jVdXWWkhKEaCpBq20ppQDh14r1jQwQCUFQpfuvOM97SslB35SvNvpzmubuu1S8QFGMwc7QfhpPFhzmHF2a278neGNrKUSSWCzE2it_4_AYabzk8kzMHkGhlUmjSipnN6XEfz3FeNiJhuzK-DQrzER6oYrLSuWoG__gd76NbhkUkIJUUtNtfqLuoERjXWDT493WdRcSC7qZJvOWmePoLJHONnOOxxsih8Q6I7QBR9jwGHfKKMm_77HWnvz0OE94c93478BcrbWpA</recordid><startdate>20131008</startdate><enddate>20131008</enddate><creator>Wang, Ning</creator><creator>Zhu, Meifen</creator><creator>Tsao, Sai-Wah</creator><creator>Man, Kwan</creator><creator>Zhang, Zhangjin</creator><creator>Feng, Yibin</creator><general>BioMed Central Ltd</general><general>BioMed Central</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>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7TM</scope><scope>5PM</scope></search><sort><creationdate>20131008</creationdate><title>MiR-23a-mediated inhibition of topoisomerase 1 expression potentiates cell response to etoposide in human hepatocellular carcinoma</title><author>Wang, Ning ; Zhu, Meifen ; Tsao, Sai-Wah ; Man, Kwan ; Zhang, Zhangjin ; Feng, Yibin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b584t-14643e30b8572b694500eaa82f9799003a3ad97188afa254eacad93c3d0d275f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>3' Untranslated Regions</topic><topic>5-Fluorouracil</topic><topic>Analysis</topic><topic>Animals</topic><topic>Antigens, Neoplasm - metabolism</topic><topic>Antineoplastic Agents, Phytogenic - pharmacology</topic><topic>Apoptosis</topic><topic>Base Sequence</topic><topic>Binding Sites</topic><topic>Cancer</topic><topic>Cancer therapies</topic><topic>Carcinoma, Hepatocellular - drug therapy</topic><topic>Carcinoma, Hepatocellular - metabolism</topic><topic>Carcinoma, Hepatocellular - pathology</topic><topic>Care and treatment</topic><topic>Cell Line, Tumor</topic><topic>Chemotherapy</topic><topic>Cytotoxicity</topic><topic>Diagnosis</topic><topic>DNA Topoisomerases, Type I - genetics</topic><topic>DNA Topoisomerases, Type I - metabolism</topic><topic>DNA Topoisomerases, Type II - metabolism</topic><topic>DNA-Binding Proteins - antagonists & inhibitors</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Drug Resistance, Neoplasm</topic><topic>Etoposide</topic><topic>Etoposide - pharmacology</topic><topic>Experiments</topic><topic>Fluorouracil</topic><topic>Fluorouracil - pharmacology</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Hepatoma</topic><topic>Humans</topic><topic>Liver cancer</topic><topic>Liver Neoplasms, Experimental - drug therapy</topic><topic>Liver Neoplasms, Experimental - metabolism</topic><topic>Liver Neoplasms, Experimental - pathology</topic><topic>Medicine</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>MicroRNA</topic><topic>MicroRNAs - genetics</topic><topic>Poly-ADP-Ribose Binding Proteins</topic><topic>Regulation</topic><topic>RNA Interference</topic><topic>Studies</topic><topic>Tumor Burden</topic><topic>Tumor proteins</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Ning</creatorcontrib><creatorcontrib>Zhu, Meifen</creatorcontrib><creatorcontrib>Tsao, Sai-Wah</creatorcontrib><creatorcontrib>Man, Kwan</creatorcontrib><creatorcontrib>Zhang, Zhangjin</creatorcontrib><creatorcontrib>Feng, Yibin</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>Oncogenes and Growth Factors Abstracts</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>ProQuest Central Essentials</collection><collection>ProQuest Central</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>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Publicly Available Content Database</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>Nucleic Acids Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Ning</au><au>Zhu, Meifen</au><au>Tsao, Sai-Wah</au><au>Man, Kwan</au><au>Zhang, Zhangjin</au><au>Feng, Yibin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MiR-23a-mediated inhibition of topoisomerase 1 expression potentiates cell response to etoposide in human hepatocellular carcinoma</atitle><jtitle>Molecular cancer</jtitle><addtitle>Mol Cancer</addtitle><date>2013-10-08</date><risdate>2013</risdate><volume>12</volume><issue>1</issue><spage>119</spage><epage>119</epage><pages>119-119</pages><artnum>119</artnum><issn>1476-4598</issn><eissn>1476-4598</eissn><abstract>microRNAs have been shown to regulate the chemosensitivity of cancer cells. The aim of this study is to investigate the role and mechanism of mir-23a in enhancing the anti-tumor effect of topoisomerase 2A (TOP2A) poison etoposide in human hepatocellular carcinoma (HCC).
The anti-tumor effect of chemotherapeutic agents in HCC cells were examined in vitro and in vivo xenograft model. Expression of mRNA and miRNAs were determined by quantitative real-time PCR. Protein expression was analyzed by immunoblotting.
Overexpression of mir-23a could significantly potentiate the in vitro and in vivo anti-tumor effect of etoposide; however, ectopic expression of miR-23a fails to sensitize HCC cells to 5-fluorouracil treatment, indicating the miR-23a-induced cancer cell hypersensitivity in chemotherapy is TOP2A-specific though miR-23a overexpression could not directly up-regulate TOP2A expression. Topoisomerase 1(TOP1) is down-regulated in miR-23a-overexpressed HCC cells. MiR-23a could directly bind to 3'untranslated region of TOP1 mRNA, and suppress the corresponding protein expression and inhibition of miR-23a further arguments the expression of TOP1. MiR-23a was up-regulated during DNA damage in cancer cells in line with the p53 expression. Up-regulation of p53 induces mir-23a expression, while suppression of p53 inhibits miR-23a in HCC cells.
Our study sheds light on the role of miR-23a as a potential target in regulating chemosensitivity of HCC cells.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>24103454</pmid><doi>10.1186/1476-4598-12-119</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 3' Untranslated Regions 5-Fluorouracil Analysis Animals Antigens, Neoplasm - metabolism Antineoplastic Agents, Phytogenic - pharmacology Apoptosis Base Sequence Binding Sites Cancer Cancer therapies Carcinoma, Hepatocellular - drug therapy Carcinoma, Hepatocellular - metabolism Carcinoma, Hepatocellular - pathology Care and treatment Cell Line, Tumor Chemotherapy Cytotoxicity Diagnosis DNA Topoisomerases, Type I - genetics DNA Topoisomerases, Type I - metabolism DNA Topoisomerases, Type II - metabolism DNA-Binding Proteins - antagonists & inhibitors DNA-Binding Proteins - metabolism Drug Resistance, Neoplasm Etoposide Etoposide - pharmacology Experiments Fluorouracil Fluorouracil - pharmacology Gene expression Gene Expression Regulation, Neoplastic Genetic aspects Health aspects Hepatoma Humans Liver cancer Liver Neoplasms, Experimental - drug therapy Liver Neoplasms, Experimental - metabolism Liver Neoplasms, Experimental - pathology Medicine Mice Mice, Inbred BALB C Mice, Nude MicroRNA MicroRNAs - genetics Poly-ADP-Ribose Binding Proteins Regulation RNA Interference Studies Tumor Burden Tumor proteins Tumor Suppressor Protein p53 - metabolism Xenograft Model Antitumor Assays |
| title | MiR-23a-mediated inhibition of topoisomerase 1 expression potentiates cell response to etoposide in human hepatocellular carcinoma |
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