miR‑425‑5p promotes cell proliferation, migration and invasion by directly targeting FOXD3 in hepatocellular carcinoma cells
MicroRNAs (miRs) are important regulators of the tumorigenesis and metastasis of various cancers. In the present study, the roles and underlying mechanisms of miR‑425‑5p in the development of hepatocellular carcinoma (HCC) were investigated. RT‑qPCR analysis revealed that miR‑425‑5p was upregulated...
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Veröffentlicht in: | Molecular medicine reports 2019-08, Vol.20 (2), p.1883-1892 |
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description | MicroRNAs (miRs) are important regulators of the tumorigenesis and metastasis of various cancers. In the present study, the roles and underlying mechanisms of miR‑425‑5p in the development of hepatocellular carcinoma (HCC) were investigated. RT‑qPCR analysis revealed that miR‑425‑5p was upregulated in HCC tissues and cell lines. A functional study in vitro using MTT assays, colony formation and Transwell assays demonstrated that overexpression of miR‑425‑5p promoted the proliferation, migration, and invasion of HCC cells, prevented cell apoptosis and accelerates the epithelial‑mesenchymal transition process, whereas miR‑425‑5p knockdown induced opposing effects. A further mechanistic study revealed that forkhead box D3 (FOXD3) was a direct target of miR‑425‑5p, and gain‑ and loss‑of‑function of FOXD3 studies demonstrated that FOXD3 suppressed HCC cell proliferation, migration, and invasion. Furthermore, rescue experiments revealed that overexpression of FOXD3 counteracted the positive effects of miR‑425‑5p on HCC malignant behaviors. Collectively, the present results demonstrated that miR‑425‑5p promoted HCC cell proliferation, migration, and invasion by suppressing FOXD3 expression, potentially providing a novel target for the treatment of HCC. |
doi_str_mv | 10.3892/mmr.2019.10427 |
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In the present study, the roles and underlying mechanisms of miR‑425‑5p in the development of hepatocellular carcinoma (HCC) were investigated. RT‑qPCR analysis revealed that miR‑425‑5p was upregulated in HCC tissues and cell lines. A functional study in vitro using MTT assays, colony formation and Transwell assays demonstrated that overexpression of miR‑425‑5p promoted the proliferation, migration, and invasion of HCC cells, prevented cell apoptosis and accelerates the epithelial‑mesenchymal transition process, whereas miR‑425‑5p knockdown induced opposing effects. A further mechanistic study revealed that forkhead box D3 (FOXD3) was a direct target of miR‑425‑5p, and gain‑ and loss‑of‑function of FOXD3 studies demonstrated that FOXD3 suppressed HCC cell proliferation, migration, and invasion. Furthermore, rescue experiments revealed that overexpression of FOXD3 counteracted the positive effects of miR‑425‑5p on HCC malignant behaviors. Collectively, the present results demonstrated that miR‑425‑5p promoted HCC cell proliferation, migration, and invasion by suppressing FOXD3 expression, potentially providing a novel target for the treatment of HCC.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2019.10427</identifier><identifier>PMID: 31257522</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Aged ; Analysis ; Apoptosis ; Biotechnology industries ; Cancer ; Cancer metastasis ; Cancer research ; Carcinogenesis - genetics ; Carcinoma ; Carcinoma, Hepatocellular - genetics ; Carcinoma, Hepatocellular - pathology ; Cell culture ; Cell growth ; Cell migration ; Cell Movement - genetics ; Cell proliferation ; Cell Proliferation - genetics ; Epithelial-Mesenchymal Transition - genetics ; Female ; Forkhead protein ; Forkhead Transcription Factors - genetics ; Gene expression ; Gene Expression Regulation, Neoplastic ; Hepatocellular carcinoma ; Humans ; Kinases ; Liver cancer ; Liver Neoplasms - genetics ; Liver Neoplasms - pathology ; Male ; Medical prognosis ; Melanoma ; Mesenchyme ; Metastases ; Metastasis ; MicroRNA ; MicroRNAs ; MicroRNAs - genetics ; Middle Aged ; miRNA ; Neoplasm Invasiveness - genetics ; Neoplasm Invasiveness - pathology ; Novels ; Patients ; Proteins ; Roles ; Scientific equipment industry ; Stem cells ; Studies ; Tumorigenesis ; Tumors ; Vascular endothelial growth factor</subject><ispartof>Molecular medicine reports, 2019-08, Vol.20 (2), p.1883-1892</ispartof><rights>COPYRIGHT 2019 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2019</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c430t-ef7f4707955b8ae4fc31a1b10f4685e2fe170b36c0943bab2552be7c2f4e080b3</citedby><cites>FETCH-LOGICAL-c430t-ef7f4707955b8ae4fc31a1b10f4685e2fe170b36c0943bab2552be7c2f4e080b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31257522$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Hewen</creatorcontrib><creatorcontrib>Shang, Jia</creatorcontrib><creatorcontrib>Zhan, Weili</creatorcontrib><creatorcontrib>Liu, Junping</creatorcontrib><creatorcontrib>Ning, Huibin</creatorcontrib><creatorcontrib>Chen, Ning</creatorcontrib><title>miR‑425‑5p promotes cell proliferation, migration and invasion by directly targeting FOXD3 in hepatocellular carcinoma cells</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>MicroRNAs (miRs) are important regulators of the tumorigenesis and metastasis of various cancers. In the present study, the roles and underlying mechanisms of miR‑425‑5p in the development of hepatocellular carcinoma (HCC) were investigated. RT‑qPCR analysis revealed that miR‑425‑5p was upregulated in HCC tissues and cell lines. A functional study in vitro using MTT assays, colony formation and Transwell assays demonstrated that overexpression of miR‑425‑5p promoted the proliferation, migration, and invasion of HCC cells, prevented cell apoptosis and accelerates the epithelial‑mesenchymal transition process, whereas miR‑425‑5p knockdown induced opposing effects. A further mechanistic study revealed that forkhead box D3 (FOXD3) was a direct target of miR‑425‑5p, and gain‑ and loss‑of‑function of FOXD3 studies demonstrated that FOXD3 suppressed HCC cell proliferation, migration, and invasion. Furthermore, rescue experiments revealed that overexpression of FOXD3 counteracted the positive effects of miR‑425‑5p on HCC malignant behaviors. Collectively, the present results demonstrated that miR‑425‑5p promoted HCC cell proliferation, migration, and invasion by suppressing FOXD3 expression, potentially providing a novel target for the treatment of HCC.</description><subject>Aged</subject><subject>Analysis</subject><subject>Apoptosis</subject><subject>Biotechnology industries</subject><subject>Cancer</subject><subject>Cancer metastasis</subject><subject>Cancer research</subject><subject>Carcinogenesis - genetics</subject><subject>Carcinoma</subject><subject>Carcinoma, Hepatocellular - genetics</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>Cell culture</subject><subject>Cell growth</subject><subject>Cell migration</subject><subject>Cell Movement - genetics</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - genetics</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>Female</subject><subject>Forkhead protein</subject><subject>Forkhead Transcription Factors - genetics</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Hepatocellular carcinoma</subject><subject>Humans</subject><subject>Kinases</subject><subject>Liver cancer</subject><subject>Liver Neoplasms - genetics</subject><subject>Liver Neoplasms - pathology</subject><subject>Male</subject><subject>Medical prognosis</subject><subject>Melanoma</subject><subject>Mesenchyme</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>Middle Aged</subject><subject>miRNA</subject><subject>Neoplasm Invasiveness - genetics</subject><subject>Neoplasm Invasiveness - pathology</subject><subject>Novels</subject><subject>Patients</subject><subject>Proteins</subject><subject>Roles</subject><subject>Scientific equipment industry</subject><subject>Stem cells</subject><subject>Studies</subject><subject>Tumorigenesis</subject><subject>Tumors</subject><subject>Vascular endothelial growth factor</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</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>eNptkVFrFDEQxxdRbK2--igBX3zwrskkuWweS21VKBSKgm8hm5ucKZvNmewK99av4FfsJzHbni1ICSQzyW9m_uHfNG8ZXfJWw3GMeQmU6SWjAtSz5pApzRacUvF8H4PW6qB5Vco1pSsJUr9sDjgDqSTAYXMTw9XtzR8Bsu5yS7Y5xTRiIQ77fs764DHbMaThI4lhcx8SO6xJGH7bMifdjqxDRjf2OzLavMExDBtyfvnjE68Q-YlbO6a539TbTJzNLgwp2rsR5XXzwtu-4Jv9edR8Pz_7dvplcXH5-evpycXCCU7HBXrlhaJKS9m1FoV3nFnWMerFqpUIHpmiHV85qgXvbAdSQofKgRdI2_py1Hy471v_9GvCMpoYyqzADpimYgAkXYGgwCr6_j_0Ok15qOpmqpVcAqWP1Mb2aMLg05itm5uaE6lVK9sWZKWWT1B1rTEGlwb0od4_VeByKiWjN9scos07w6iZLTfVcjNbbu4srwXv9mqnLuL6Af_nMf8LnCWoGA</recordid><startdate>20190801</startdate><enddate>20190801</enddate><creator>Wu, Hewen</creator><creator>Shang, Jia</creator><creator>Zhan, Weili</creator><creator>Liu, Junping</creator><creator>Ning, Huibin</creator><creator>Chen, Ning</creator><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>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</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>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20190801</creationdate><title>miR‑425‑5p promotes cell proliferation, migration and invasion by directly targeting FOXD3 in hepatocellular carcinoma cells</title><author>Wu, Hewen ; Shang, Jia ; Zhan, Weili ; Liu, Junping ; Ning, Huibin ; Chen, Ning</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c430t-ef7f4707955b8ae4fc31a1b10f4685e2fe170b36c0943bab2552be7c2f4e080b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Aged</topic><topic>Analysis</topic><topic>Apoptosis</topic><topic>Biotechnology industries</topic><topic>Cancer</topic><topic>Cancer metastasis</topic><topic>Cancer research</topic><topic>Carcinogenesis - genetics</topic><topic>Carcinoma</topic><topic>Carcinoma, Hepatocellular - genetics</topic><topic>Carcinoma, Hepatocellular - pathology</topic><topic>Cell culture</topic><topic>Cell growth</topic><topic>Cell migration</topic><topic>Cell Movement - genetics</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - genetics</topic><topic>Epithelial-Mesenchymal Transition - genetics</topic><topic>Female</topic><topic>Forkhead protein</topic><topic>Forkhead Transcription Factors - genetics</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Hepatocellular carcinoma</topic><topic>Humans</topic><topic>Kinases</topic><topic>Liver cancer</topic><topic>Liver Neoplasms - genetics</topic><topic>Liver Neoplasms - pathology</topic><topic>Male</topic><topic>Medical prognosis</topic><topic>Melanoma</topic><topic>Mesenchyme</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>MicroRNA</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>Middle Aged</topic><topic>miRNA</topic><topic>Neoplasm Invasiveness - 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Academic</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Hewen</au><au>Shang, Jia</au><au>Zhan, Weili</au><au>Liu, Junping</au><au>Ning, Huibin</au><au>Chen, Ning</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR‑425‑5p promotes cell proliferation, migration and invasion by directly targeting FOXD3 in hepatocellular carcinoma cells</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2019-08-01</date><risdate>2019</risdate><volume>20</volume><issue>2</issue><spage>1883</spage><epage>1892</epage><pages>1883-1892</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>MicroRNAs (miRs) are important regulators of the tumorigenesis and metastasis of various cancers. In the present study, the roles and underlying mechanisms of miR‑425‑5p in the development of hepatocellular carcinoma (HCC) were investigated. RT‑qPCR analysis revealed that miR‑425‑5p was upregulated in HCC tissues and cell lines. A functional study in vitro using MTT assays, colony formation and Transwell assays demonstrated that overexpression of miR‑425‑5p promoted the proliferation, migration, and invasion of HCC cells, prevented cell apoptosis and accelerates the epithelial‑mesenchymal transition process, whereas miR‑425‑5p knockdown induced opposing effects. A further mechanistic study revealed that forkhead box D3 (FOXD3) was a direct target of miR‑425‑5p, and gain‑ and loss‑of‑function of FOXD3 studies demonstrated that FOXD3 suppressed HCC cell proliferation, migration, and invasion. Furthermore, rescue experiments revealed that overexpression of FOXD3 counteracted the positive effects of miR‑425‑5p on HCC malignant behaviors. Collectively, the present results demonstrated that miR‑425‑5p promoted HCC cell proliferation, migration, and invasion by suppressing FOXD3 expression, potentially providing a novel target for the treatment of HCC.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>31257522</pmid><doi>10.3892/mmr.2019.10427</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Aged Analysis Apoptosis Biotechnology industries Cancer Cancer metastasis Cancer research Carcinogenesis - genetics Carcinoma Carcinoma, Hepatocellular - genetics Carcinoma, Hepatocellular - pathology Cell culture Cell growth Cell migration Cell Movement - genetics Cell proliferation Cell Proliferation - genetics Epithelial-Mesenchymal Transition - genetics Female Forkhead protein Forkhead Transcription Factors - genetics Gene expression Gene Expression Regulation, Neoplastic Hepatocellular carcinoma Humans Kinases Liver cancer Liver Neoplasms - genetics Liver Neoplasms - pathology Male Medical prognosis Melanoma Mesenchyme Metastases Metastasis MicroRNA MicroRNAs MicroRNAs - genetics Middle Aged miRNA Neoplasm Invasiveness - genetics Neoplasm Invasiveness - pathology Novels Patients Proteins Roles Scientific equipment industry Stem cells Studies Tumorigenesis Tumors Vascular endothelial growth factor |
title | miR‑425‑5p promotes cell proliferation, migration and invasion by directly targeting FOXD3 in hepatocellular carcinoma cells |
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