Functional mechanism and clinical implications of MicroRNA‐423 in human cancers
MicroRNAs play a vital role in the regulatory mechanisms of tumorigenesis. Current research indicates that microRNA‐423 (miR‐423) is abnormally expressed in various human tumors and participates in multiple signaling pathways of cancer progression. In most studies, miR‐423 was confirmed as oncomiR,...
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Veröffentlicht in: | Cancer medicine (Malden, MA) MA), 2020-12, Vol.9 (23), p.9036-9051 |
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description | MicroRNAs play a vital role in the regulatory mechanisms of tumorigenesis. Current research indicates that microRNA‐423 (miR‐423) is abnormally expressed in various human tumors and participates in multiple signaling pathways of cancer progression. In most studies, miR‐423 was confirmed as oncomiR, while a few contradictory reports considered miR‐423 as an anticancer miRNA. The paradoxical role in cancer may hinder the application of miR‐423 as a diagnostic and therapeutic target. Simultaneously, the interaction mechanism between miR‐423 and lncRNA also needs attention. In this review, we have summarized the dual role of aberrant miR‐423 expression and its mechanisms in tumorigenesis, and the therapeutic potential of miR‐423 in human tumors.
Has‐microRNA‐423 (miR‐423) is abnormally expressed in various human tumors and plays a role in cancer progression. Abnormal expression of miR‐423 may have dual effects, and actively exploring its mechanism in tumorigenesis may contribute to the treatment of tumors. Increasing evidence suggests that miR‐423 may serve as a biomarker for early diagnosis and prognostic monitoring of human cancers. |
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Has‐microRNA‐423 (miR‐423) is abnormally expressed in various human tumors and plays a role in cancer progression. Abnormal expression of miR‐423 may have dual effects, and actively exploring its mechanism in tumorigenesis may contribute to the treatment of tumors. Increasing evidence suggests that miR‐423 may serve as a biomarker for early diagnosis and prognostic monitoring of human cancers.</description><identifier>ISSN: 2045-7634</identifier><identifier>EISSN: 2045-7634</identifier><identifier>DOI: 10.1002/cam4.3557</identifier><identifier>PMID: 33174687</identifier><language>eng</language><publisher>United States: John Wiley & Sons, Inc</publisher><subject>Cancer Biology ; Carcinogens ; Cell growth ; clinical implications ; Endometrial cancer ; functional mechanism ; MicroRNAs ; MicroRNA‐423 ; miRNA ; Ovarian cancer ; Review ; Tumorigenesis</subject><ispartof>Cancer medicine (Malden, MA), 2020-12, Vol.9 (23), p.9036-9051</ispartof><rights>2020 The Authors. published by John Wiley & Sons Ltd.</rights><rights>2020 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.</rights><rights>2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4437-e14b8a13c2f4fe178df178693f00bd43880d3c4bc3fad6d0977f9ffbe567d24b3</citedby><cites>FETCH-LOGICAL-c4437-e14b8a13c2f4fe178df178693f00bd43880d3c4bc3fad6d0977f9ffbe567d24b3</cites><orcidid>0000-0001-9269-4692</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/PMC7724490/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7724490/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1417,11562,27924,27925,45574,45575,46052,46476,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33174687$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ke, RuiSheng</creatorcontrib><creatorcontrib>Lv, LiZhi</creatorcontrib><creatorcontrib>Zhang, SiYu</creatorcontrib><creatorcontrib>Zhang, FuXing</creatorcontrib><creatorcontrib>Jiang, Yi</creatorcontrib><title>Functional mechanism and clinical implications of MicroRNA‐423 in human cancers</title><title>Cancer medicine (Malden, MA)</title><addtitle>Cancer Med</addtitle><description>MicroRNAs play a vital role in the regulatory mechanisms of tumorigenesis. Current research indicates that microRNA‐423 (miR‐423) is abnormally expressed in various human tumors and participates in multiple signaling pathways of cancer progression. In most studies, miR‐423 was confirmed as oncomiR, while a few contradictory reports considered miR‐423 as an anticancer miRNA. The paradoxical role in cancer may hinder the application of miR‐423 as a diagnostic and therapeutic target. Simultaneously, the interaction mechanism between miR‐423 and lncRNA also needs attention. In this review, we have summarized the dual role of aberrant miR‐423 expression and its mechanisms in tumorigenesis, and the therapeutic potential of miR‐423 in human tumors.
Has‐microRNA‐423 (miR‐423) is abnormally expressed in various human tumors and plays a role in cancer progression. Abnormal expression of miR‐423 may have dual effects, and actively exploring its mechanism in tumorigenesis may contribute to the treatment of tumors. Increasing evidence suggests that miR‐423 may serve as a biomarker for early diagnosis and prognostic monitoring of human cancers.</description><subject>Cancer Biology</subject><subject>Carcinogens</subject><subject>Cell growth</subject><subject>clinical implications</subject><subject>Endometrial cancer</subject><subject>functional mechanism</subject><subject>MicroRNAs</subject><subject>MicroRNA‐423</subject><subject>miRNA</subject><subject>Ovarian cancer</subject><subject>Review</subject><subject>Tumorigenesis</subject><issn>2045-7634</issn><issn>2045-7634</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kdFKwzAUhoMobsxd-AJS8EYvtqVJ2rQ3whhOhU1R9DqkaeIy2nQmq7I7H8Fn9ElM3RxTMBfJ4eTj43B-AI5D2A8hRAPBS9LHUUT3QBtBEvVojMn-Tt0CXefm0B8KUUzDQ9DCOKQkTmgb3I9rI5a6MrwISilm3GhXBtzkgSi00cK3dbkofNFALqhUMNXCVg-3w8_3D4JwoE0wq0tuAsGNkNYdgQPFCye7m7cDnsaXj6Pr3uTu6mY0nPQEIZj2ZEiyhIdYIEWUDGmSK3_FKVYQZjnBSQJzLEgmsOJ5nMOUUpUqlckopjkiGe6Ai7V3UWelzIU0S8sLtrC65HbFKq7Z7x-jZ-y5emWUIkJS6AVnG4GtXmrplqzUTsii4EZWtWOIRGmMaIIa9PQPOq9q63fWUHECKUYR9dT5mvL7cc5KtR0mhKzJijVZsSYrz57sTr8lf5LxwGANvOlCrv43sdFwSr6VX_rznnc</recordid><startdate>202012</startdate><enddate>202012</enddate><creator>Ke, RuiSheng</creator><creator>Lv, LiZhi</creator><creator>Zhang, SiYu</creator><creator>Zhang, FuXing</creator><creator>Jiang, Yi</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</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>M7P</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/0000-0001-9269-4692</orcidid></search><sort><creationdate>202012</creationdate><title>Functional mechanism and clinical implications of MicroRNA‐423 in human cancers</title><author>Ke, RuiSheng ; Lv, LiZhi ; Zhang, SiYu ; Zhang, FuXing ; Jiang, Yi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4437-e14b8a13c2f4fe178df178693f00bd43880d3c4bc3fad6d0977f9ffbe567d24b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Cancer Biology</topic><topic>Carcinogens</topic><topic>Cell growth</topic><topic>clinical implications</topic><topic>Endometrial cancer</topic><topic>functional mechanism</topic><topic>MicroRNAs</topic><topic>MicroRNA‐423</topic><topic>miRNA</topic><topic>Ovarian cancer</topic><topic>Review</topic><topic>Tumorigenesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ke, RuiSheng</creatorcontrib><creatorcontrib>Lv, LiZhi</creatorcontrib><creatorcontrib>Zhang, SiYu</creatorcontrib><creatorcontrib>Zhang, FuXing</creatorcontrib><creatorcontrib>Jiang, Yi</creatorcontrib><collection>Wiley-Blackwell Open Access Titles</collection><collection>Wiley Free Content</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>ProQuest SciTech 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>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</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>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Biological Science 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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer medicine (Malden, MA)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ke, RuiSheng</au><au>Lv, LiZhi</au><au>Zhang, SiYu</au><au>Zhang, FuXing</au><au>Jiang, Yi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Functional mechanism and clinical implications of MicroRNA‐423 in human cancers</atitle><jtitle>Cancer medicine (Malden, MA)</jtitle><addtitle>Cancer Med</addtitle><date>2020-12</date><risdate>2020</risdate><volume>9</volume><issue>23</issue><spage>9036</spage><epage>9051</epage><pages>9036-9051</pages><issn>2045-7634</issn><eissn>2045-7634</eissn><abstract>MicroRNAs play a vital role in the regulatory mechanisms of tumorigenesis. Current research indicates that microRNA‐423 (miR‐423) is abnormally expressed in various human tumors and participates in multiple signaling pathways of cancer progression. In most studies, miR‐423 was confirmed as oncomiR, while a few contradictory reports considered miR‐423 as an anticancer miRNA. The paradoxical role in cancer may hinder the application of miR‐423 as a diagnostic and therapeutic target. Simultaneously, the interaction mechanism between miR‐423 and lncRNA also needs attention. In this review, we have summarized the dual role of aberrant miR‐423 expression and its mechanisms in tumorigenesis, and the therapeutic potential of miR‐423 in human tumors.
Has‐microRNA‐423 (miR‐423) is abnormally expressed in various human tumors and plays a role in cancer progression. Abnormal expression of miR‐423 may have dual effects, and actively exploring its mechanism in tumorigenesis may contribute to the treatment of tumors. Increasing evidence suggests that miR‐423 may serve as a biomarker for early diagnosis and prognostic monitoring of human cancers.</abstract><cop>United States</cop><pub>John Wiley & Sons, Inc</pub><pmid>33174687</pmid><doi>10.1002/cam4.3557</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0001-9269-4692</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Cancer Biology Carcinogens Cell growth clinical implications Endometrial cancer functional mechanism MicroRNAs MicroRNA‐423 miRNA Ovarian cancer Review Tumorigenesis |
title | Functional mechanism and clinical implications of MicroRNA‐423 in human cancers |
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