MiR-221 Promotes Hepatocellular Carcinoma Cells Migration via Targeting PHF2
MicroRNAs (MiRNAs), which regulate the gene expression leading to translational inhibition or mRNA degradation, are involved in carcinogenesis and tumor progression. Previous studies have demonstrated that miR-221 was one of the most consistent overexpressed miRNAs in several types of cancer. Howeve...
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| Veröffentlicht in: | BioMed research international 2019-01, Vol.2019 (2019), p.1-11 |
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| creator | Hou, Ruixing Lv, Fengwei Zhang, Ping Qian, Li Li, Fengxia Liu, Mingyan Fu, Yi Cheng, Wenting |
| description | MicroRNAs (MiRNAs), which regulate the gene expression leading to translational inhibition or mRNA degradation, are involved in carcinogenesis and tumor progression. Previous studies have demonstrated that miR-221 was one of the most consistent overexpressed miRNAs in several types of cancer. However, the role of miR-221 in human liver cancer progression is not yet fully elucidated. Levels of miR-221 and plant homeodomain finger 2 (PHF2) expressions in human hepatocellular carcinoma (HCC) tissues and cell lines were detected using western blotting and quantitative real-time PCR (qRT-PCR). Cell migration was studied using the transwell assays. A dual-luciferase reporter system was used to validate the target gene of miR-221. The results indicated that miR-221 promoted HCC cell migration. By performing subsequent systematic bioinformatic analyses, we found PHF2 was the target gene of miR-221 and the direct binding relationship was further validated by dual-luciferase reporter assay. In addition, lower expression of PHF2 promoted HCC cell migration and linked to worse overall survival in HCC patients. Finally, the negative correlation between miR-221 and PHF2 expression levels in HCC specimens was further confirmed. Taken together, our findings implied that miR-221 could be a potential candidate for the therapeutics of HCC metastasis. |
| doi_str_mv | 10.1155/2019/4371405 |
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Previous studies have demonstrated that miR-221 was one of the most consistent overexpressed miRNAs in several types of cancer. However, the role of miR-221 in human liver cancer progression is not yet fully elucidated. Levels of miR-221 and plant homeodomain finger 2 (PHF2) expressions in human hepatocellular carcinoma (HCC) tissues and cell lines were detected using western blotting and quantitative real-time PCR (qRT-PCR). Cell migration was studied using the transwell assays. A dual-luciferase reporter system was used to validate the target gene of miR-221. The results indicated that miR-221 promoted HCC cell migration. By performing subsequent systematic bioinformatic analyses, we found PHF2 was the target gene of miR-221 and the direct binding relationship was further validated by dual-luciferase reporter assay. In addition, lower expression of PHF2 promoted HCC cell migration and linked to worse overall survival in HCC patients. Finally, the negative correlation between miR-221 and PHF2 expression levels in HCC specimens was further confirmed. Taken together, our findings implied that miR-221 could be a potential candidate for the therapeutics of HCC metastasis.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2019/4371405</identifier><identifier>PMID: 31214616</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Apoptosis ; Biomedical research ; Breast cancer ; Carcinogenesis ; Carcinogens ; Carcinoma, Hepatocellular - genetics ; Carcinoma, Hepatocellular - metabolism ; Carcinoma, Hepatocellular - pathology ; Cell adhesion & migration ; Cell cycle ; Cell migration ; Cell Movement ; Development and progression ; Drug therapy ; Female ; Gene expression ; Gene Expression Regulation, Neoplastic ; Genes ; Hep G2 Cells ; Hepatocellular carcinoma ; Hepatoma ; Homeobox ; Homeodomain Proteins - biosynthesis ; Homeodomain Proteins - genetics ; Hospitals ; Humans ; Kidney cancer ; Liver cancer ; Liver Neoplasms - genetics ; Liver Neoplasms - metabolism ; Liver Neoplasms - pathology ; Male ; Medical research ; Metastases ; Metastasis ; MicroRNA ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; Mutation ; Neoplasm Metastasis ; Neoplasm Proteins - biosynthesis ; Neoplasm Proteins - genetics ; Proteins ; RNA, Neoplasm - genetics ; RNA, Neoplasm - metabolism ; Studies ; Tumor cell lines ; Tumorigenesis ; Western blotting</subject><ispartof>BioMed research international, 2019-01, Vol.2019 (2019), p.1-11</ispartof><rights>Copyright © 2019 Yi Fu et al.</rights><rights>COPYRIGHT 2019 John Wiley & Sons, Inc.</rights><rights>Copyright © 2019 Yi Fu et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2019 Yi Fu et al. 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-843ea37b415ffafadad9e8e03e3077f0ca8291918f0f03d81367b45f174092e23</citedby><cites>FETCH-LOGICAL-c499t-843ea37b415ffafadad9e8e03e3077f0ca8291918f0f03d81367b45f174092e23</cites><orcidid>0000-0002-5257-0684 ; 0000-0001-9913-5623</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6535842/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6535842/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27915,27916,53782,53784</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31214616$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Imazeki, Fumio</contributor><contributor>Fumio Imazeki</contributor><creatorcontrib>Hou, Ruixing</creatorcontrib><creatorcontrib>Lv, Fengwei</creatorcontrib><creatorcontrib>Zhang, Ping</creatorcontrib><creatorcontrib>Qian, Li</creatorcontrib><creatorcontrib>Li, Fengxia</creatorcontrib><creatorcontrib>Liu, Mingyan</creatorcontrib><creatorcontrib>Fu, Yi</creatorcontrib><creatorcontrib>Cheng, Wenting</creatorcontrib><title>MiR-221 Promotes Hepatocellular Carcinoma Cells Migration via Targeting PHF2</title><title>BioMed research international</title><addtitle>Biomed Res Int</addtitle><description>MicroRNAs (MiRNAs), which regulate the gene expression leading to translational inhibition or mRNA degradation, are involved in carcinogenesis and tumor progression. Previous studies have demonstrated that miR-221 was one of the most consistent overexpressed miRNAs in several types of cancer. However, the role of miR-221 in human liver cancer progression is not yet fully elucidated. Levels of miR-221 and plant homeodomain finger 2 (PHF2) expressions in human hepatocellular carcinoma (HCC) tissues and cell lines were detected using western blotting and quantitative real-time PCR (qRT-PCR). Cell migration was studied using the transwell assays. A dual-luciferase reporter system was used to validate the target gene of miR-221. The results indicated that miR-221 promoted HCC cell migration. By performing subsequent systematic bioinformatic analyses, we found PHF2 was the target gene of miR-221 and the direct binding relationship was further validated by dual-luciferase reporter assay. In addition, lower expression of PHF2 promoted HCC cell migration and linked to worse overall survival in HCC patients. Finally, the negative correlation between miR-221 and PHF2 expression levels in HCC specimens was further confirmed. Taken together, our findings implied that miR-221 could be a potential candidate for the therapeutics of HCC metastasis.</description><subject>Apoptosis</subject><subject>Biomedical research</subject><subject>Breast cancer</subject><subject>Carcinogenesis</subject><subject>Carcinogens</subject><subject>Carcinoma, Hepatocellular - genetics</subject><subject>Carcinoma, Hepatocellular - metabolism</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>Cell adhesion & migration</subject><subject>Cell cycle</subject><subject>Cell migration</subject><subject>Cell Movement</subject><subject>Development and progression</subject><subject>Drug therapy</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes</subject><subject>Hep G2 Cells</subject><subject>Hepatocellular carcinoma</subject><subject>Hepatoma</subject><subject>Homeobox</subject><subject>Homeodomain Proteins - biosynthesis</subject><subject>Homeodomain Proteins - genetics</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Kidney cancer</subject><subject>Liver cancer</subject><subject>Liver Neoplasms - genetics</subject><subject>Liver Neoplasms - metabolism</subject><subject>Liver Neoplasms - pathology</subject><subject>Male</subject><subject>Medical research</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Mutation</subject><subject>Neoplasm Metastasis</subject><subject>Neoplasm Proteins - biosynthesis</subject><subject>Neoplasm Proteins - genetics</subject><subject>Proteins</subject><subject>RNA, Neoplasm - genetics</subject><subject>RNA, Neoplasm - metabolism</subject><subject>Studies</subject><subject>Tumor cell lines</subject><subject>Tumorigenesis</subject><subject>Western blotting</subject><issn>2314-6133</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><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>eNqNkdFr1TAUh4sobsy9-SwFXwRXl5OTtM2LMC7OK9zhkPkcztqky2iba9JO_O-Xcq936pN5SUg-vpwfvyx7DewDgJTnnIE6F1iBYPJZdswRRFGCgOeHM-JRdhrjPUurhpKp8mV2hMBBlFAeZ5sr963gHPLr4Ac_mZivzZYm35i-n3sK-YpC40Y_UL5KVzG_cl2gyfkxf3CU31DozOTGLr9eX_JX2QtLfTSn-_0k-3756Wa1LjZfP39ZXWyKRig1FbVAQ1jdCpDWkqWWWmVqw9AgqyrLGqq5AgW1ZZZhWwOWCZYWKsEUNxxPso8773a-HUzbmHEK1OttcAOFX9qT03-_jO5Od_5BlxJlLRbBu70g-B-ziZMeXFwi02j8HDXnAoWSiU7o23_Qez-HMcVLFDKOCCieqI56o91offq3WaT6InUgmZJ8cZ3tqCb4GIOxh5GB6aVPvfSp930m_M2fMQ_w7_YS8H4H3LmxpZ_uP3UmMcbSEw1pNqjwEbOXrhU</recordid><startdate>20190101</startdate><enddate>20190101</enddate><creator>Hou, Ruixing</creator><creator>Lv, Fengwei</creator><creator>Zhang, Ping</creator><creator>Qian, Li</creator><creator>Li, Fengxia</creator><creator>Liu, Mingyan</creator><creator>Fu, Yi</creator><creator>Cheng, Wenting</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><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>7QL</scope><scope>7QO</scope><scope>7T7</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>CWDGH</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-5257-0684</orcidid><orcidid>https://orcid.org/0000-0001-9913-5623</orcidid></search><sort><creationdate>20190101</creationdate><title>MiR-221 Promotes Hepatocellular Carcinoma Cells Migration via Targeting PHF2</title><author>Hou, Ruixing ; Lv, Fengwei ; Zhang, Ping ; Qian, Li ; Li, Fengxia ; Liu, Mingyan ; Fu, Yi ; Cheng, Wenting</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c499t-843ea37b415ffafadad9e8e03e3077f0ca8291918f0f03d81367b45f174092e23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Apoptosis</topic><topic>Biomedical research</topic><topic>Breast cancer</topic><topic>Carcinogenesis</topic><topic>Carcinogens</topic><topic>Carcinoma, Hepatocellular - genetics</topic><topic>Carcinoma, Hepatocellular - metabolism</topic><topic>Carcinoma, Hepatocellular - pathology</topic><topic>Cell adhesion & migration</topic><topic>Cell cycle</topic><topic>Cell migration</topic><topic>Cell Movement</topic><topic>Development and progression</topic><topic>Drug therapy</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes</topic><topic>Hep G2 Cells</topic><topic>Hepatocellular carcinoma</topic><topic>Hepatoma</topic><topic>Homeobox</topic><topic>Homeodomain Proteins - biosynthesis</topic><topic>Homeodomain Proteins - genetics</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Kidney cancer</topic><topic>Liver cancer</topic><topic>Liver Neoplasms - genetics</topic><topic>Liver Neoplasms - metabolism</topic><topic>Liver Neoplasms - pathology</topic><topic>Male</topic><topic>Medical research</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>MicroRNA</topic><topic>MicroRNAs</topic><topic>MicroRNAs - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BioMed research international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hou, Ruixing</au><au>Lv, Fengwei</au><au>Zhang, Ping</au><au>Qian, Li</au><au>Li, Fengxia</au><au>Liu, Mingyan</au><au>Fu, Yi</au><au>Cheng, Wenting</au><au>Imazeki, Fumio</au><au>Fumio Imazeki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MiR-221 Promotes Hepatocellular Carcinoma Cells Migration via Targeting PHF2</atitle><jtitle>BioMed research international</jtitle><addtitle>Biomed Res Int</addtitle><date>2019-01-01</date><risdate>2019</risdate><volume>2019</volume><issue>2019</issue><spage>1</spage><epage>11</epage><pages>1-11</pages><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>MicroRNAs (MiRNAs), which regulate the gene expression leading to translational inhibition or mRNA degradation, are involved in carcinogenesis and tumor progression. Previous studies have demonstrated that miR-221 was one of the most consistent overexpressed miRNAs in several types of cancer. However, the role of miR-221 in human liver cancer progression is not yet fully elucidated. Levels of miR-221 and plant homeodomain finger 2 (PHF2) expressions in human hepatocellular carcinoma (HCC) tissues and cell lines were detected using western blotting and quantitative real-time PCR (qRT-PCR). Cell migration was studied using the transwell assays. A dual-luciferase reporter system was used to validate the target gene of miR-221. The results indicated that miR-221 promoted HCC cell migration. By performing subsequent systematic bioinformatic analyses, we found PHF2 was the target gene of miR-221 and the direct binding relationship was further validated by dual-luciferase reporter assay. In addition, lower expression of PHF2 promoted HCC cell migration and linked to worse overall survival in HCC patients. Finally, the negative correlation between miR-221 and PHF2 expression levels in HCC specimens was further confirmed. Taken together, our findings implied that miR-221 could be a potential candidate for the therapeutics of HCC metastasis.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>31214616</pmid><doi>10.1155/2019/4371405</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-5257-0684</orcidid><orcidid>https://orcid.org/0000-0001-9913-5623</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Apoptosis Biomedical research Breast cancer Carcinogenesis Carcinogens Carcinoma, Hepatocellular - genetics Carcinoma, Hepatocellular - metabolism Carcinoma, Hepatocellular - pathology Cell adhesion & migration Cell cycle Cell migration Cell Movement Development and progression Drug therapy Female Gene expression Gene Expression Regulation, Neoplastic Genes Hep G2 Cells Hepatocellular carcinoma Hepatoma Homeobox Homeodomain Proteins - biosynthesis Homeodomain Proteins - genetics Hospitals Humans Kidney cancer Liver cancer Liver Neoplasms - genetics Liver Neoplasms - metabolism Liver Neoplasms - pathology Male Medical research Metastases Metastasis MicroRNA MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism miRNA Mutation Neoplasm Metastasis Neoplasm Proteins - biosynthesis Neoplasm Proteins - genetics Proteins RNA, Neoplasm - genetics RNA, Neoplasm - metabolism Studies Tumor cell lines Tumorigenesis Western blotting |
| title | MiR-221 Promotes Hepatocellular Carcinoma Cells Migration via Targeting PHF2 |
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