MiR-122 directly inhibits human papillomavirus E6 gene and enhances interferon signaling through blocking suppressor of cytokine signaling 1 in SiHa cells
Human Papillomavirus (HPV) 16 infection is considered as one of the significant causes of human cervical cancer. The expression of the viral oncogenes like E6 and E7 play an important role in the development of the cancer. MiR-122 has been reported to exhibit a strong relationship with hepatitis vir...
Gespeichert in:
| Veröffentlicht in: | PloS one 2014-09, Vol.9 (9), p.e108410-e108410 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | e108410 |
|---|---|
| container_issue | 9 |
| container_start_page | e108410 |
| container_title | PloS one |
| container_volume | 9 |
| creator | He, Junming Ji, Yuting Li, Aimei Zhang, Qingmeng Song, Wuqi Li, Yujun Huang, Hongxin Qian, Jun Zhai, Aixia Yu, Xin Zhao, Jinyun Shang, Qinglong Wei, Lanlan Zhang, Fengmin |
| description | Human Papillomavirus (HPV) 16 infection is considered as one of the significant causes of human cervical cancer. The expression of the viral oncogenes like E6 and E7 play an important role in the development of the cancer. MiR-122 has been reported to exhibit a strong relationship with hepatitis viruses and take part in several tumor development, while the effects of miR-122 on HPV infection and the HPV viral oncogenes expression still remain unexplored. In this study, using RNAhybrid software, the potential binding sites between miR-122 and HPV16 E6 and E7 mRNAs were identified. Over and loss of miR-122 function showed that miR-122 could directly bind with HPV16 E6 mRNA and significantly inhibit its expression in SiHa cells, which was further confirmed by constructing the miR-122-E6-mu to eliminate the miR-122 binding effects with E6. The increase of the expression of type I interferon (IFN) and its classical effective molecules and the phosphorylation of signal transducers and activators of transcription (STAT1) protein indicated that miR-122 might enhance type I interferon in cervical carcinoma cells, which explained the significant reduction of HPV16 E7 and E6*I mRNA expression. This might be due to the binding between miR-122 and suppressor of cytokine signaling 1 (SOCS1) mRNA, which is the suppressor of interferon signaling pathway. Moreover, it was identified that the miR-122 binding position was nt359-nt375 in SOCS1 mRNA. Taken together, this study indicated that HPV16 could be effectively inhibited by miR-122 through both direct binding with E6 mRNA and promoting SOCS1-dependent IFN signaling pathway. Thus, miR-122 may serve as a new therapeutic option for inhibiting HPV infection. |
| doi_str_mv | 10.1371/journal.pone.0108410 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_plos_</sourceid><recordid>TN_cdi_plos_journals_1566321903</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><doaj_id>oai_doaj_org_article_568ab407f38b4bb4b0587dd8544e1c43</doaj_id><sourcerecordid>3446929171</sourcerecordid><originalsourceid>FETCH-LOGICAL-c526t-d6d4eae11d6fca327ffa36f345712d3311985c79c862d8f2efee225441a851153</originalsourceid><addsrcrecordid>eNptUltrFDEYHUSxtfoPRAO-9GXXfLlN9kWQ0tpCRfDyHDKZb2ayziZjMlPYv-Kvddbdlq0IgYSTc8534RTFa6BL4CW8X8cpBdsvhxhwSYFqAfRJcQorzhaKUf706H1SvMh5TankWqnnxQmTTEkK_LT4_dl_XQBjpPYJ3dhviQ-dr_yYSTdtbCCDHXzfx42982nK5FKRFgMSG2qCobPBYZ4lI6YGUwwk-3ZuyoeWjF2KU9uRqo_u5w7I0zAkzDkmEhvitmOcYTxSwGxEvvlrSxz2fX5ZPGtsn_HV4T4rflxdfr-4Xtx--XRz8fF24eYpxkWtaoEWAWrVOMtZ2TSWq4YLWQKrOQdYaenKldOK1bph2CAyJoUAqyWA5GfF273v0MdsDmvNBqRSnMGK8plxs2fU0a7NkPzGpq2J1pu_QEytsWn0rkcjlbaVoGXDdSWq-VCpy7rWcz0EJ3ZeHw7VpmqDtcMwJts_Mn38E3xn2nhnBGhaSjEbnB8MUvw1YR7NxufdwmzAOO371oyC0DP13T_U_08n9iyXYs4Jm4dmgJpd1O5VZhc1c4jaLHtzPMiD6D5b_A-f4tPt</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1566321903</pqid></control><display><type>article</type><title>MiR-122 directly inhibits human papillomavirus E6 gene and enhances interferon signaling through blocking suppressor of cytokine signaling 1 in SiHa cells</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Public Library of Science (PLoS) Journals Open Access</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Free Full-Text Journals in Chemistry</source><creator>He, Junming ; Ji, Yuting ; Li, Aimei ; Zhang, Qingmeng ; Song, Wuqi ; Li, Yujun ; Huang, Hongxin ; Qian, Jun ; Zhai, Aixia ; Yu, Xin ; Zhao, Jinyun ; Shang, Qinglong ; Wei, Lanlan ; Zhang, Fengmin</creator><contributor>Rottenberg, Martin E.</contributor><creatorcontrib>He, Junming ; Ji, Yuting ; Li, Aimei ; Zhang, Qingmeng ; Song, Wuqi ; Li, Yujun ; Huang, Hongxin ; Qian, Jun ; Zhai, Aixia ; Yu, Xin ; Zhao, Jinyun ; Shang, Qinglong ; Wei, Lanlan ; Zhang, Fengmin ; Rottenberg, Martin E.</creatorcontrib><description>Human Papillomavirus (HPV) 16 infection is considered as one of the significant causes of human cervical cancer. The expression of the viral oncogenes like E6 and E7 play an important role in the development of the cancer. MiR-122 has been reported to exhibit a strong relationship with hepatitis viruses and take part in several tumor development, while the effects of miR-122 on HPV infection and the HPV viral oncogenes expression still remain unexplored. In this study, using RNAhybrid software, the potential binding sites between miR-122 and HPV16 E6 and E7 mRNAs were identified. Over and loss of miR-122 function showed that miR-122 could directly bind with HPV16 E6 mRNA and significantly inhibit its expression in SiHa cells, which was further confirmed by constructing the miR-122-E6-mu to eliminate the miR-122 binding effects with E6. The increase of the expression of type I interferon (IFN) and its classical effective molecules and the phosphorylation of signal transducers and activators of transcription (STAT1) protein indicated that miR-122 might enhance type I interferon in cervical carcinoma cells, which explained the significant reduction of HPV16 E7 and E6*I mRNA expression. This might be due to the binding between miR-122 and suppressor of cytokine signaling 1 (SOCS1) mRNA, which is the suppressor of interferon signaling pathway. Moreover, it was identified that the miR-122 binding position was nt359-nt375 in SOCS1 mRNA. Taken together, this study indicated that HPV16 could be effectively inhibited by miR-122 through both direct binding with E6 mRNA and promoting SOCS1-dependent IFN signaling pathway. Thus, miR-122 may serve as a new therapeutic option for inhibiting HPV infection.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0108410</identifier><identifier>PMID: 25265013</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Binding sites ; Binding Sites - genetics ; Biology ; Biology and Life Sciences ; Cancer ; Cell Line, Tumor ; Cervical cancer ; Cervical carcinoma ; Cervix ; Cytokines ; E6 gene ; Female ; Gene expression ; Genomes ; HeLa Cells ; Hepatitis ; Higher education ; Human papillomavirus ; Humans ; Infections ; Inhibition ; Interferon ; Interferon Type I - metabolism ; Kinases ; Laboratories ; MicroRNAs ; MicroRNAs - biosynthesis ; MicroRNAs - genetics ; Oncogene Proteins, Viral - antagonists & inhibitors ; Oncogene Proteins, Viral - genetics ; Papillomavirus E7 Proteins - genetics ; Papillomavirus Infections - virology ; Phosphorylation ; Plasmids ; Proteins ; Repressor Proteins - antagonists & inhibitors ; Repressor Proteins - genetics ; RNA, Messenger - biosynthesis ; RNA, Messenger - genetics ; RNA, Viral - biosynthesis ; RNA, Viral - genetics ; Signal transduction ; Signaling ; SOCS-1 protein ; Stat1 protein ; STAT1 Transcription Factor - metabolism ; Stem cells ; Suppressor of Cytokine Signaling 1 Protein ; Suppressor of Cytokine Signaling Proteins - antagonists & inhibitors ; Transcription ; Transcription factors ; Transducers ; Uterine Cervical Neoplasms - virology ; Viral infections ; Viruses</subject><ispartof>PloS one, 2014-09, Vol.9 (9), p.e108410-e108410</ispartof><rights>2014 He et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 He et al 2014 He et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c526t-d6d4eae11d6fca327ffa36f345712d3311985c79c862d8f2efee225441a851153</citedby><cites>FETCH-LOGICAL-c526t-d6d4eae11d6fca327ffa36f345712d3311985c79c862d8f2efee225441a851153</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/PMC4180754/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4180754/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25265013$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Rottenberg, Martin E.</contributor><creatorcontrib>He, Junming</creatorcontrib><creatorcontrib>Ji, Yuting</creatorcontrib><creatorcontrib>Li, Aimei</creatorcontrib><creatorcontrib>Zhang, Qingmeng</creatorcontrib><creatorcontrib>Song, Wuqi</creatorcontrib><creatorcontrib>Li, Yujun</creatorcontrib><creatorcontrib>Huang, Hongxin</creatorcontrib><creatorcontrib>Qian, Jun</creatorcontrib><creatorcontrib>Zhai, Aixia</creatorcontrib><creatorcontrib>Yu, Xin</creatorcontrib><creatorcontrib>Zhao, Jinyun</creatorcontrib><creatorcontrib>Shang, Qinglong</creatorcontrib><creatorcontrib>Wei, Lanlan</creatorcontrib><creatorcontrib>Zhang, Fengmin</creatorcontrib><title>MiR-122 directly inhibits human papillomavirus E6 gene and enhances interferon signaling through blocking suppressor of cytokine signaling 1 in SiHa cells</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Human Papillomavirus (HPV) 16 infection is considered as one of the significant causes of human cervical cancer. The expression of the viral oncogenes like E6 and E7 play an important role in the development of the cancer. MiR-122 has been reported to exhibit a strong relationship with hepatitis viruses and take part in several tumor development, while the effects of miR-122 on HPV infection and the HPV viral oncogenes expression still remain unexplored. In this study, using RNAhybrid software, the potential binding sites between miR-122 and HPV16 E6 and E7 mRNAs were identified. Over and loss of miR-122 function showed that miR-122 could directly bind with HPV16 E6 mRNA and significantly inhibit its expression in SiHa cells, which was further confirmed by constructing the miR-122-E6-mu to eliminate the miR-122 binding effects with E6. The increase of the expression of type I interferon (IFN) and its classical effective molecules and the phosphorylation of signal transducers and activators of transcription (STAT1) protein indicated that miR-122 might enhance type I interferon in cervical carcinoma cells, which explained the significant reduction of HPV16 E7 and E6*I mRNA expression. This might be due to the binding between miR-122 and suppressor of cytokine signaling 1 (SOCS1) mRNA, which is the suppressor of interferon signaling pathway. Moreover, it was identified that the miR-122 binding position was nt359-nt375 in SOCS1 mRNA. Taken together, this study indicated that HPV16 could be effectively inhibited by miR-122 through both direct binding with E6 mRNA and promoting SOCS1-dependent IFN signaling pathway. Thus, miR-122 may serve as a new therapeutic option for inhibiting HPV infection.</description><subject>Binding sites</subject><subject>Binding Sites - genetics</subject><subject>Biology</subject><subject>Biology and Life Sciences</subject><subject>Cancer</subject><subject>Cell Line, Tumor</subject><subject>Cervical cancer</subject><subject>Cervical carcinoma</subject><subject>Cervix</subject><subject>Cytokines</subject><subject>E6 gene</subject><subject>Female</subject><subject>Gene expression</subject><subject>Genomes</subject><subject>HeLa Cells</subject><subject>Hepatitis</subject><subject>Higher education</subject><subject>Human papillomavirus</subject><subject>Humans</subject><subject>Infections</subject><subject>Inhibition</subject><subject>Interferon</subject><subject>Interferon Type I - metabolism</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>MicroRNAs</subject><subject>MicroRNAs - biosynthesis</subject><subject>MicroRNAs - genetics</subject><subject>Oncogene Proteins, Viral - antagonists & inhibitors</subject><subject>Oncogene Proteins, Viral - genetics</subject><subject>Papillomavirus E7 Proteins - genetics</subject><subject>Papillomavirus Infections - virology</subject><subject>Phosphorylation</subject><subject>Plasmids</subject><subject>Proteins</subject><subject>Repressor Proteins - antagonists & inhibitors</subject><subject>Repressor Proteins - genetics</subject><subject>RNA, Messenger - biosynthesis</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Viral - biosynthesis</subject><subject>RNA, Viral - genetics</subject><subject>Signal transduction</subject><subject>Signaling</subject><subject>SOCS-1 protein</subject><subject>Stat1 protein</subject><subject>STAT1 Transcription Factor - metabolism</subject><subject>Stem cells</subject><subject>Suppressor of Cytokine Signaling 1 Protein</subject><subject>Suppressor of Cytokine Signaling Proteins - antagonists & inhibitors</subject><subject>Transcription</subject><subject>Transcription factors</subject><subject>Transducers</subject><subject>Uterine Cervical Neoplasms - virology</subject><subject>Viral infections</subject><subject>Viruses</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</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><sourceid>DOA</sourceid><recordid>eNptUltrFDEYHUSxtfoPRAO-9GXXfLlN9kWQ0tpCRfDyHDKZb2ayziZjMlPYv-Kvddbdlq0IgYSTc8534RTFa6BL4CW8X8cpBdsvhxhwSYFqAfRJcQorzhaKUf706H1SvMh5TankWqnnxQmTTEkK_LT4_dl_XQBjpPYJ3dhviQ-dr_yYSTdtbCCDHXzfx42982nK5FKRFgMSG2qCobPBYZ4lI6YGUwwk-3ZuyoeWjF2KU9uRqo_u5w7I0zAkzDkmEhvitmOcYTxSwGxEvvlrSxz2fX5ZPGtsn_HV4T4rflxdfr-4Xtx--XRz8fF24eYpxkWtaoEWAWrVOMtZ2TSWq4YLWQKrOQdYaenKldOK1bph2CAyJoUAqyWA5GfF273v0MdsDmvNBqRSnMGK8plxs2fU0a7NkPzGpq2J1pu_QEytsWn0rkcjlbaVoGXDdSWq-VCpy7rWcz0EJ3ZeHw7VpmqDtcMwJts_Mn38E3xn2nhnBGhaSjEbnB8MUvw1YR7NxufdwmzAOO371oyC0DP13T_U_08n9iyXYs4Jm4dmgJpd1O5VZhc1c4jaLHtzPMiD6D5b_A-f4tPt</recordid><startdate>20140929</startdate><enddate>20140929</enddate><creator>He, Junming</creator><creator>Ji, Yuting</creator><creator>Li, Aimei</creator><creator>Zhang, Qingmeng</creator><creator>Song, Wuqi</creator><creator>Li, Yujun</creator><creator>Huang, Hongxin</creator><creator>Qian, Jun</creator><creator>Zhai, Aixia</creator><creator>Yu, Xin</creator><creator>Zhao, Jinyun</creator><creator>Shang, Qinglong</creator><creator>Wei, Lanlan</creator><creator>Zhang, Fengmin</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</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>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20140929</creationdate><title>MiR-122 directly inhibits human papillomavirus E6 gene and enhances interferon signaling through blocking suppressor of cytokine signaling 1 in SiHa cells</title><author>He, Junming ; Ji, Yuting ; Li, Aimei ; Zhang, Qingmeng ; Song, Wuqi ; Li, Yujun ; Huang, Hongxin ; Qian, Jun ; Zhai, Aixia ; Yu, Xin ; Zhao, Jinyun ; Shang, Qinglong ; Wei, Lanlan ; Zhang, Fengmin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c526t-d6d4eae11d6fca327ffa36f345712d3311985c79c862d8f2efee225441a851153</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Binding sites</topic><topic>Binding Sites - genetics</topic><topic>Biology</topic><topic>Biology and Life Sciences</topic><topic>Cancer</topic><topic>Cell Line, Tumor</topic><topic>Cervical cancer</topic><topic>Cervical carcinoma</topic><topic>Cervix</topic><topic>Cytokines</topic><topic>E6 gene</topic><topic>Female</topic><topic>Gene expression</topic><topic>Genomes</topic><topic>HeLa Cells</topic><topic>Hepatitis</topic><topic>Higher education</topic><topic>Human papillomavirus</topic><topic>Humans</topic><topic>Infections</topic><topic>Inhibition</topic><topic>Interferon</topic><topic>Interferon Type I - metabolism</topic><topic>Kinases</topic><topic>Laboratories</topic><topic>MicroRNAs</topic><topic>MicroRNAs - biosynthesis</topic><topic>MicroRNAs - genetics</topic><topic>Oncogene Proteins, Viral - antagonists & inhibitors</topic><topic>Oncogene Proteins, Viral - genetics</topic><topic>Papillomavirus E7 Proteins - genetics</topic><topic>Papillomavirus Infections - virology</topic><topic>Phosphorylation</topic><topic>Plasmids</topic><topic>Proteins</topic><topic>Repressor Proteins - antagonists & inhibitors</topic><topic>Repressor Proteins - genetics</topic><topic>RNA, Messenger - biosynthesis</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Viral - biosynthesis</topic><topic>RNA, Viral - genetics</topic><topic>Signal transduction</topic><topic>Signaling</topic><topic>SOCS-1 protein</topic><topic>Stat1 protein</topic><topic>STAT1 Transcription Factor - metabolism</topic><topic>Stem cells</topic><topic>Suppressor of Cytokine Signaling 1 Protein</topic><topic>Suppressor of Cytokine Signaling Proteins - antagonists & inhibitors</topic><topic>Transcription</topic><topic>Transcription factors</topic><topic>Transducers</topic><topic>Uterine Cervical Neoplasms - virology</topic><topic>Viral infections</topic><topic>Viruses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>He, Junming</creatorcontrib><creatorcontrib>Ji, Yuting</creatorcontrib><creatorcontrib>Li, Aimei</creatorcontrib><creatorcontrib>Zhang, Qingmeng</creatorcontrib><creatorcontrib>Song, Wuqi</creatorcontrib><creatorcontrib>Li, Yujun</creatorcontrib><creatorcontrib>Huang, Hongxin</creatorcontrib><creatorcontrib>Qian, Jun</creatorcontrib><creatorcontrib>Zhai, Aixia</creatorcontrib><creatorcontrib>Yu, Xin</creatorcontrib><creatorcontrib>Zhao, Jinyun</creatorcontrib><creatorcontrib>Shang, Qinglong</creatorcontrib><creatorcontrib>Wei, Lanlan</creatorcontrib><creatorcontrib>Zhang, Fengmin</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>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Access via ProQuest (Open Access)</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>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>He, Junming</au><au>Ji, Yuting</au><au>Li, Aimei</au><au>Zhang, Qingmeng</au><au>Song, Wuqi</au><au>Li, Yujun</au><au>Huang, Hongxin</au><au>Qian, Jun</au><au>Zhai, Aixia</au><au>Yu, Xin</au><au>Zhao, Jinyun</au><au>Shang, Qinglong</au><au>Wei, Lanlan</au><au>Zhang, Fengmin</au><au>Rottenberg, Martin E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MiR-122 directly inhibits human papillomavirus E6 gene and enhances interferon signaling through blocking suppressor of cytokine signaling 1 in SiHa cells</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-09-29</date><risdate>2014</risdate><volume>9</volume><issue>9</issue><spage>e108410</spage><epage>e108410</epage><pages>e108410-e108410</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Human Papillomavirus (HPV) 16 infection is considered as one of the significant causes of human cervical cancer. The expression of the viral oncogenes like E6 and E7 play an important role in the development of the cancer. MiR-122 has been reported to exhibit a strong relationship with hepatitis viruses and take part in several tumor development, while the effects of miR-122 on HPV infection and the HPV viral oncogenes expression still remain unexplored. In this study, using RNAhybrid software, the potential binding sites between miR-122 and HPV16 E6 and E7 mRNAs were identified. Over and loss of miR-122 function showed that miR-122 could directly bind with HPV16 E6 mRNA and significantly inhibit its expression in SiHa cells, which was further confirmed by constructing the miR-122-E6-mu to eliminate the miR-122 binding effects with E6. The increase of the expression of type I interferon (IFN) and its classical effective molecules and the phosphorylation of signal transducers and activators of transcription (STAT1) protein indicated that miR-122 might enhance type I interferon in cervical carcinoma cells, which explained the significant reduction of HPV16 E7 and E6*I mRNA expression. This might be due to the binding between miR-122 and suppressor of cytokine signaling 1 (SOCS1) mRNA, which is the suppressor of interferon signaling pathway. Moreover, it was identified that the miR-122 binding position was nt359-nt375 in SOCS1 mRNA. Taken together, this study indicated that HPV16 could be effectively inhibited by miR-122 through both direct binding with E6 mRNA and promoting SOCS1-dependent IFN signaling pathway. Thus, miR-122 may serve as a new therapeutic option for inhibiting HPV infection.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25265013</pmid><doi>10.1371/journal.pone.0108410</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2014-09, Vol.9 (9), p.e108410-e108410 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1566321903 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Binding sites Binding Sites - genetics Biology Biology and Life Sciences Cancer Cell Line, Tumor Cervical cancer Cervical carcinoma Cervix Cytokines E6 gene Female Gene expression Genomes HeLa Cells Hepatitis Higher education Human papillomavirus Humans Infections Inhibition Interferon Interferon Type I - metabolism Kinases Laboratories MicroRNAs MicroRNAs - biosynthesis MicroRNAs - genetics Oncogene Proteins, Viral - antagonists & inhibitors Oncogene Proteins, Viral - genetics Papillomavirus E7 Proteins - genetics Papillomavirus Infections - virology Phosphorylation Plasmids Proteins Repressor Proteins - antagonists & inhibitors Repressor Proteins - genetics RNA, Messenger - biosynthesis RNA, Messenger - genetics RNA, Viral - biosynthesis RNA, Viral - genetics Signal transduction Signaling SOCS-1 protein Stat1 protein STAT1 Transcription Factor - metabolism Stem cells Suppressor of Cytokine Signaling 1 Protein Suppressor of Cytokine Signaling Proteins - antagonists & inhibitors Transcription Transcription factors Transducers Uterine Cervical Neoplasms - virology Viral infections Viruses |
| title | MiR-122 directly inhibits human papillomavirus E6 gene and enhances interferon signaling through blocking suppressor of cytokine signaling 1 in SiHa cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-19T17%3A12%3A14IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=MiR-122%20directly%20inhibits%20human%20papillomavirus%20E6%20gene%20and%20enhances%20interferon%20signaling%20through%20blocking%20suppressor%20of%20cytokine%20signaling%201%20in%20SiHa%20cells&rft.jtitle=PloS%20one&rft.au=He,%20Junming&rft.date=2014-09-29&rft.volume=9&rft.issue=9&rft.spage=e108410&rft.epage=e108410&rft.pages=e108410-e108410&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0108410&rft_dat=%3Cproquest_plos_%3E3446929171%3C/proquest_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1566321903&rft_id=info:pmid/25265013&rft_doaj_id=oai_doaj_org_article_568ab407f38b4bb4b0587dd8544e1c43&rfr_iscdi=true |