p53-induced microRNA-1246 inhibits the cell growth of human hepatocellular carcinoma cells by targeting NFIB
In recent years, miR-1246 has been identified as a transcriptional target of p53 in Down syndrome and may provide a new p53-miR-1246-DYRK1A-NFAT pathway in cancer. The present study aimed to explore the role of miR-1246 in the tumorigenesis of human hepatocellular carcinoma (HCC). We found that wild...
Gespeichert in:
| Veröffentlicht in: | Oncology reports 2015-03, Vol.33 (3), p.1335-1341 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1341 |
|---|---|
| container_issue | 3 |
| container_start_page | 1335 |
| container_title | Oncology reports |
| container_volume | 33 |
| creator | ZHANG, QUAN CAO, LI-YE CHENG, SHU-JIE ZHANG, AI-MIN JIN, XIAO-SHI LI, YONG |
| description | In recent years, miR-1246 has been identified as a transcriptional target of p53 in Down syndrome and may provide a new p53-miR-1246-DYRK1A-NFAT pathway in cancer. The present study aimed to explore the role of miR-1246 in the tumorigenesis of human hepatocellular carcinoma (HCC). We found that wild-type p53 regulated the expression of miR-1246 in HCC cell lines, and alteration of miR-1246 modulated cell proliferation, colony formation ability and apoptosis. The nuclear factor I/B (NFIB), an oncogene, was identified as a direct target gene of miR-1246 using a fluorescent reporter assay. Overexpression of NFIB abolished the regulation of cell apoptosis caused by miR-1246 in HepG2 cells. This finding suggests that miR-1246 is regulated by p53 and suppresses the growth of human HCC by targeting NFIB. Here, we propose a new p53-miR-1246-NFIB pathway in HCC. |
| doi_str_mv | 10.3892/or.2015.3715 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_1652444854</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A407905074</galeid><sourcerecordid>A407905074</sourcerecordid><originalsourceid>FETCH-LOGICAL-c552t-db4a3ef587478956e035e906e14511aef135d793fc8fa07c5797f77f5a0f900f3</originalsourceid><addsrcrecordid>eNptkl1rFTEQhhdR7IfeeS0BQXrhHjP52GwuT4vVQqkgCt6FnN3kbMpusiZZpP_erK2tFclFQuaZNzOZt6peAd7QVpL3IW4IBr6hAviT6hCEhJowCk_LGROoKeXfD6qjlK4xJgI38nl1QDiX0BI4rMaZ09r5fulMjybXxfDlalsDYQ1yfnA7lxPKg0GdGUe0j-FnHlCwaFgm7dFgZp3DGlpGHVGnY-d8mPRvOqHdDco67k12fo-uzi9OX1TPrB6TeXm3H1ffzj98PftUX37-eHG2vaw7zkmu-x3T1FjeCiZayRuDKTcSNwYYB9DGAuW9kNR2rdVYdFxIYYWwXGMrMbb0uDq51Z1j-LGYlNXk0lqT9iYsSUHDCWOs5aygb_5Br8MSfalOgaSkabls4YHa69Eo523IUXerqNoyLCTmWKxam_9QZfWm_Gzwxrpy_yjh7V8Jg9FjHlIYl-yCT4_Bd7dgmU9K0Vg1RzfpeKMAq9UFKkS1ukCtLij467umlt1k-nv4z9gfHk6z9r3rQ7pnQiyOqTGtoRiH_gLYLrVR</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1932685981</pqid></control><display><type>article</type><title>p53-induced microRNA-1246 inhibits the cell growth of human hepatocellular carcinoma cells by targeting NFIB</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>ZHANG, QUAN ; CAO, LI-YE ; CHENG, SHU-JIE ; ZHANG, AI-MIN ; JIN, XIAO-SHI ; LI, YONG</creator><creatorcontrib>ZHANG, QUAN ; CAO, LI-YE ; CHENG, SHU-JIE ; ZHANG, AI-MIN ; JIN, XIAO-SHI ; LI, YONG</creatorcontrib><description>In recent years, miR-1246 has been identified as a transcriptional target of p53 in Down syndrome and may provide a new p53-miR-1246-DYRK1A-NFAT pathway in cancer. The present study aimed to explore the role of miR-1246 in the tumorigenesis of human hepatocellular carcinoma (HCC). We found that wild-type p53 regulated the expression of miR-1246 in HCC cell lines, and alteration of miR-1246 modulated cell proliferation, colony formation ability and apoptosis. The nuclear factor I/B (NFIB), an oncogene, was identified as a direct target gene of miR-1246 using a fluorescent reporter assay. Overexpression of NFIB abolished the regulation of cell apoptosis caused by miR-1246 in HepG2 cells. This finding suggests that miR-1246 is regulated by p53 and suppresses the growth of human HCC by targeting NFIB. Here, we propose a new p53-miR-1246-NFIB pathway in HCC.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2015.3715</identifier><identifier>PMID: 25591821</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Apoptosis ; Apoptosis - genetics ; Breast cancer ; Carcinoma, Hepatocellular - genetics ; Cell growth ; Cell Line, Tumor ; Cell proliferation ; Cell Proliferation - genetics ; Cell Transformation, Neoplastic - genetics ; Development and progression ; Gene expression ; Gene Expression Regulation, Neoplastic ; HCC ; Health aspects ; Hep G2 Cells ; Hepatoma ; Humans ; Kinases ; Laboratories ; Liver cancer ; Liver Neoplasms - genetics ; MicroRNA ; MicroRNAs - biosynthesis ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miR-1246 ; NFI Transcription Factors - biosynthesis ; NFI Transcription Factors - genetics ; NFI Transcription Factors - metabolism ; NFIB ; Oncogenes ; Prevention ; RNA Interference ; RNA, Small Interfering ; Statistical analysis ; Transcription factors ; Tumor proteins ; Tumor Suppressor Protein p53 - genetics ; Tumor Suppressor Protein p53 - metabolism</subject><ispartof>Oncology reports, 2015-03, Vol.33 (3), p.1335-1341</ispartof><rights>Copyright © 2015, Spandidos Publications</rights><rights>COPYRIGHT 2015 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c552t-db4a3ef587478956e035e906e14511aef135d793fc8fa07c5797f77f5a0f900f3</citedby><cites>FETCH-LOGICAL-c552t-db4a3ef587478956e035e906e14511aef135d793fc8fa07c5797f77f5a0f900f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25591821$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>ZHANG, QUAN</creatorcontrib><creatorcontrib>CAO, LI-YE</creatorcontrib><creatorcontrib>CHENG, SHU-JIE</creatorcontrib><creatorcontrib>ZHANG, AI-MIN</creatorcontrib><creatorcontrib>JIN, XIAO-SHI</creatorcontrib><creatorcontrib>LI, YONG</creatorcontrib><title>p53-induced microRNA-1246 inhibits the cell growth of human hepatocellular carcinoma cells by targeting NFIB</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>In recent years, miR-1246 has been identified as a transcriptional target of p53 in Down syndrome and may provide a new p53-miR-1246-DYRK1A-NFAT pathway in cancer. The present study aimed to explore the role of miR-1246 in the tumorigenesis of human hepatocellular carcinoma (HCC). We found that wild-type p53 regulated the expression of miR-1246 in HCC cell lines, and alteration of miR-1246 modulated cell proliferation, colony formation ability and apoptosis. The nuclear factor I/B (NFIB), an oncogene, was identified as a direct target gene of miR-1246 using a fluorescent reporter assay. Overexpression of NFIB abolished the regulation of cell apoptosis caused by miR-1246 in HepG2 cells. This finding suggests that miR-1246 is regulated by p53 and suppresses the growth of human HCC by targeting NFIB. Here, we propose a new p53-miR-1246-NFIB pathway in HCC.</description><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Breast cancer</subject><subject>Carcinoma, Hepatocellular - genetics</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - genetics</subject><subject>Cell Transformation, Neoplastic - genetics</subject><subject>Development and progression</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>HCC</subject><subject>Health aspects</subject><subject>Hep G2 Cells</subject><subject>Hepatoma</subject><subject>Humans</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Liver cancer</subject><subject>Liver Neoplasms - genetics</subject><subject>MicroRNA</subject><subject>MicroRNAs - biosynthesis</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miR-1246</subject><subject>NFI Transcription Factors - biosynthesis</subject><subject>NFI Transcription Factors - genetics</subject><subject>NFI Transcription Factors - metabolism</subject><subject>NFIB</subject><subject>Oncogenes</subject><subject>Prevention</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering</subject><subject>Statistical analysis</subject><subject>Transcription factors</subject><subject>Tumor proteins</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptkl1rFTEQhhdR7IfeeS0BQXrhHjP52GwuT4vVQqkgCt6FnN3kbMpusiZZpP_erK2tFclFQuaZNzOZt6peAd7QVpL3IW4IBr6hAviT6hCEhJowCk_LGROoKeXfD6qjlK4xJgI38nl1QDiX0BI4rMaZ09r5fulMjybXxfDlalsDYQ1yfnA7lxPKg0GdGUe0j-FnHlCwaFgm7dFgZp3DGlpGHVGnY-d8mPRvOqHdDco67k12fo-uzi9OX1TPrB6TeXm3H1ffzj98PftUX37-eHG2vaw7zkmu-x3T1FjeCiZayRuDKTcSNwYYB9DGAuW9kNR2rdVYdFxIYYWwXGMrMbb0uDq51Z1j-LGYlNXk0lqT9iYsSUHDCWOs5aygb_5Br8MSfalOgaSkabls4YHa69Eo523IUXerqNoyLCTmWKxam_9QZfWm_Gzwxrpy_yjh7V8Jg9FjHlIYl-yCT4_Bd7dgmU9K0Vg1RzfpeKMAq9UFKkS1ukCtLij467umlt1k-nv4z9gfHk6z9r3rQ7pnQiyOqTGtoRiH_gLYLrVR</recordid><startdate>20150301</startdate><enddate>20150301</enddate><creator>ZHANG, QUAN</creator><creator>CAO, LI-YE</creator><creator>CHENG, SHU-JIE</creator><creator>ZHANG, AI-MIN</creator><creator>JIN, XIAO-SHI</creator><creator>LI, YONG</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20150301</creationdate><title>p53-induced microRNA-1246 inhibits the cell growth of human hepatocellular carcinoma cells by targeting NFIB</title><author>ZHANG, QUAN ; CAO, LI-YE ; CHENG, SHU-JIE ; ZHANG, AI-MIN ; JIN, XIAO-SHI ; LI, YONG</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c552t-db4a3ef587478956e035e906e14511aef135d793fc8fa07c5797f77f5a0f900f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Breast cancer</topic><topic>Carcinoma, Hepatocellular - genetics</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - genetics</topic><topic>Cell Transformation, Neoplastic - genetics</topic><topic>Development and progression</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>HCC</topic><topic>Health aspects</topic><topic>Hep G2 Cells</topic><topic>Hepatoma</topic><topic>Humans</topic><topic>Kinases</topic><topic>Laboratories</topic><topic>Liver cancer</topic><topic>Liver Neoplasms - genetics</topic><topic>MicroRNA</topic><topic>MicroRNAs - biosynthesis</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miR-1246</topic><topic>NFI Transcription Factors - biosynthesis</topic><topic>NFI Transcription Factors - genetics</topic><topic>NFI Transcription Factors - metabolism</topic><topic>NFIB</topic><topic>Oncogenes</topic><topic>Prevention</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering</topic><topic>Statistical analysis</topic><topic>Transcription factors</topic><topic>Tumor proteins</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>ZHANG, QUAN</creatorcontrib><creatorcontrib>CAO, LI-YE</creatorcontrib><creatorcontrib>CHENG, SHU-JIE</creatorcontrib><creatorcontrib>ZHANG, AI-MIN</creatorcontrib><creatorcontrib>JIN, XIAO-SHI</creatorcontrib><creatorcontrib>LI, YONG</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>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>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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>MEDLINE - Academic</collection><jtitle>Oncology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>ZHANG, QUAN</au><au>CAO, LI-YE</au><au>CHENG, SHU-JIE</au><au>ZHANG, AI-MIN</au><au>JIN, XIAO-SHI</au><au>LI, YONG</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>p53-induced microRNA-1246 inhibits the cell growth of human hepatocellular carcinoma cells by targeting NFIB</atitle><jtitle>Oncology reports</jtitle><addtitle>Oncol Rep</addtitle><date>2015-03-01</date><risdate>2015</risdate><volume>33</volume><issue>3</issue><spage>1335</spage><epage>1341</epage><pages>1335-1341</pages><issn>1021-335X</issn><eissn>1791-2431</eissn><abstract>In recent years, miR-1246 has been identified as a transcriptional target of p53 in Down syndrome and may provide a new p53-miR-1246-DYRK1A-NFAT pathway in cancer. The present study aimed to explore the role of miR-1246 in the tumorigenesis of human hepatocellular carcinoma (HCC). We found that wild-type p53 regulated the expression of miR-1246 in HCC cell lines, and alteration of miR-1246 modulated cell proliferation, colony formation ability and apoptosis. The nuclear factor I/B (NFIB), an oncogene, was identified as a direct target gene of miR-1246 using a fluorescent reporter assay. Overexpression of NFIB abolished the regulation of cell apoptosis caused by miR-1246 in HepG2 cells. This finding suggests that miR-1246 is regulated by p53 and suppresses the growth of human HCC by targeting NFIB. Here, we propose a new p53-miR-1246-NFIB pathway in HCC.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>25591821</pmid><doi>10.3892/or.2015.3715</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1021-335X |
| ispartof | Oncology reports, 2015-03, Vol.33 (3), p.1335-1341 |
| issn | 1021-335X 1791-2431 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1652444854 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Apoptosis Apoptosis - genetics Breast cancer Carcinoma, Hepatocellular - genetics Cell growth Cell Line, Tumor Cell proliferation Cell Proliferation - genetics Cell Transformation, Neoplastic - genetics Development and progression Gene expression Gene Expression Regulation, Neoplastic HCC Health aspects Hep G2 Cells Hepatoma Humans Kinases Laboratories Liver cancer Liver Neoplasms - genetics MicroRNA MicroRNAs - biosynthesis MicroRNAs - genetics MicroRNAs - metabolism miR-1246 NFI Transcription Factors - biosynthesis NFI Transcription Factors - genetics NFI Transcription Factors - metabolism NFIB Oncogenes Prevention RNA Interference RNA, Small Interfering Statistical analysis Transcription factors Tumor proteins Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism |
| title | p53-induced microRNA-1246 inhibits the cell growth of human hepatocellular carcinoma cells by targeting NFIB |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-03T04%3A00%3A50IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=p53-induced%20microRNA-1246%20inhibits%20the%20cell%20growth%20of%20human%20hepatocellular%20carcinoma%20cells%20by%20targeting%20NFIB&rft.jtitle=Oncology%20reports&rft.au=ZHANG,%20QUAN&rft.date=2015-03-01&rft.volume=33&rft.issue=3&rft.spage=1335&rft.epage=1341&rft.pages=1335-1341&rft.issn=1021-335X&rft.eissn=1791-2431&rft_id=info:doi/10.3892/or.2015.3715&rft_dat=%3Cgale_proqu%3EA407905074%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1932685981&rft_id=info:pmid/25591821&rft_galeid=A407905074&rfr_iscdi=true |