STAT3 activates the transcription of lncRNA NR2F1-AS1 to promote the progression of melanoma via regulating the miR-493-5p/GOLM1 axis
Long non-coding RNAs (lncRNAs) are vital regulators during the biological processes of melanoma. The present study aimed to uncover biological functions of lncRNA termed NR2F1 antisense RNA 1 (NR2F1-AS1) in melanoma and the potential mechanisms. Relative levels of NR2F1-AS1 and miR-493-5p in a total...
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| Veröffentlicht in: | The journal of gene medicine 2021-07, Vol.23 (7), p.e3338-e3338 |
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| creator | Bai, Mei Wu, Zong-Zhou Huang, Yan-Li Ke, Jin Xu, Qing Wang, Xiong |
| description | Long non-coding RNAs (lncRNAs) are vital regulators during the biological processes of melanoma. The present study aimed to uncover biological functions of lncRNA termed NR2F1 antisense RNA 1 (NR2F1-AS1) in melanoma and the potential mechanisms.
Relative levels of NR2F1-AS1 and miR-493-5p in a total of 137 paired primary melanoma tissues and corresponding non-tumor tissues, as well as three melanoma cell lines, were examined by a real-time polymerase chain reaction. The clinical significance of NR2F1-AS1 expression was analyzed statistically. The STAT3 binding motif in the promoter region of NR2F1-AS1 was identified by JASPAR (http://jaspar.genereg.net). The association between STAT3 and NR2F1-AS1 was determined by dual-luciferase reporter and chromatin immunoprecipitation assays. The effects of NR2F1-AS1 on cell proliferation, migration and were measured by cell counting kit-8 (CCK-8), Edu, transwell and wound healing assays. Dual-luciferase reporter and RNA pull-down assays were applied to validate the interaction among NR2F1-AS1, miR-493-5p and GOLM1. Furthermore, in vivo experiments were conducted to demonstrate the oncogenic role of NR2F1-AS1 in melanoma.
Up-regulated NR2F1-AS1 and down-regulated miR-493-5p were detected in melanoma tumors and cells. The overexpression of NR2F1-AS1 was induced by STAT3. High NR2F1-AS1 expression was correlated to advanced tumor stage and poor prognosis of melanoma. Functional studies using CCK-8, Edu, transwell and wound healing assays revealed that the proliferative, migratory and invasive capacities of melanoma cells were attenuated by the by inhibition of NR2F1-AS1. Moreover, NR2F1-AS1 was able to up-regulate GOLM1 through recognizing and binding miR-493-5p. Furthermore, knockdown of miR-493-5p distinctly reversed these inhibitory effects of NR2F1-AS1 down-regulation on the tumorigenesis and progression of melanoma.
Our findings demonstrate a key role for NR2F1-AS1 in melanoma progression via targeting miR-493-5p/GOLM1 axis. |
| doi_str_mv | 10.1002/jgm.3338 |
| format | Article |
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Relative levels of NR2F1-AS1 and miR-493-5p in a total of 137 paired primary melanoma tissues and corresponding non-tumor tissues, as well as three melanoma cell lines, were examined by a real-time polymerase chain reaction. The clinical significance of NR2F1-AS1 expression was analyzed statistically. The STAT3 binding motif in the promoter region of NR2F1-AS1 was identified by JASPAR (http://jaspar.genereg.net). The association between STAT3 and NR2F1-AS1 was determined by dual-luciferase reporter and chromatin immunoprecipitation assays. The effects of NR2F1-AS1 on cell proliferation, migration and were measured by cell counting kit-8 (CCK-8), Edu, transwell and wound healing assays. Dual-luciferase reporter and RNA pull-down assays were applied to validate the interaction among NR2F1-AS1, miR-493-5p and GOLM1. Furthermore, in vivo experiments were conducted to demonstrate the oncogenic role of NR2F1-AS1 in melanoma.
Up-regulated NR2F1-AS1 and down-regulated miR-493-5p were detected in melanoma tumors and cells. The overexpression of NR2F1-AS1 was induced by STAT3. High NR2F1-AS1 expression was correlated to advanced tumor stage and poor prognosis of melanoma. Functional studies using CCK-8, Edu, transwell and wound healing assays revealed that the proliferative, migratory and invasive capacities of melanoma cells were attenuated by the by inhibition of NR2F1-AS1. Moreover, NR2F1-AS1 was able to up-regulate GOLM1 through recognizing and binding miR-493-5p. Furthermore, knockdown of miR-493-5p distinctly reversed these inhibitory effects of NR2F1-AS1 down-regulation on the tumorigenesis and progression of melanoma.
Our findings demonstrate a key role for NR2F1-AS1 in melanoma progression via targeting miR-493-5p/GOLM1 axis.</description><identifier>ISSN: 1099-498X</identifier><identifier>EISSN: 1521-2254</identifier><identifier>DOI: 10.1002/jgm.3338</identifier><identifier>PMID: 33822440</identifier><language>eng</language><publisher>England: Wiley Periodicals Inc</publisher><subject>Antisense RNA ; Cell Line, Tumor ; Cell migration ; Cell Movement ; Cell Proliferation ; Cholecystokinin ; Chromatin ; COUP Transcription Factor I - genetics ; COUP Transcription Factor I - metabolism ; Disease Progression ; Gene Expression Regulation, Neoplastic ; Gene therapy ; Humans ; Immunoprecipitation ; Melanoma ; Melanoma - genetics ; Melanoma - metabolism ; Membrane Proteins - metabolism ; MicroRNAs - metabolism ; Non-coding RNA ; Polymerase chain reaction ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; Signal Transduction ; Stat3 protein ; STAT3 Transcription Factor - genetics ; Transcription ; Tumorigenesis ; Wound healing</subject><ispartof>The journal of gene medicine, 2021-07, Vol.23 (7), p.e3338-e3338</ispartof><rights>2021 John Wiley & Sons, Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c311t-9792a2d06a1dd3f30ac804b71324e57d15f235f07e019a0540633d60f3f2ba4e3</citedby><cites>FETCH-LOGICAL-c311t-9792a2d06a1dd3f30ac804b71324e57d15f235f07e019a0540633d60f3f2ba4e3</cites><orcidid>0000-0002-9778-7377</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27915,27916</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33822440$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bai, Mei</creatorcontrib><creatorcontrib>Wu, Zong-Zhou</creatorcontrib><creatorcontrib>Huang, Yan-Li</creatorcontrib><creatorcontrib>Ke, Jin</creatorcontrib><creatorcontrib>Xu, Qing</creatorcontrib><creatorcontrib>Wang, Xiong</creatorcontrib><title>STAT3 activates the transcription of lncRNA NR2F1-AS1 to promote the progression of melanoma via regulating the miR-493-5p/GOLM1 axis</title><title>The journal of gene medicine</title><addtitle>J Gene Med</addtitle><description>Long non-coding RNAs (lncRNAs) are vital regulators during the biological processes of melanoma. The present study aimed to uncover biological functions of lncRNA termed NR2F1 antisense RNA 1 (NR2F1-AS1) in melanoma and the potential mechanisms.
Relative levels of NR2F1-AS1 and miR-493-5p in a total of 137 paired primary melanoma tissues and corresponding non-tumor tissues, as well as three melanoma cell lines, were examined by a real-time polymerase chain reaction. The clinical significance of NR2F1-AS1 expression was analyzed statistically. The STAT3 binding motif in the promoter region of NR2F1-AS1 was identified by JASPAR (http://jaspar.genereg.net). The association between STAT3 and NR2F1-AS1 was determined by dual-luciferase reporter and chromatin immunoprecipitation assays. The effects of NR2F1-AS1 on cell proliferation, migration and were measured by cell counting kit-8 (CCK-8), Edu, transwell and wound healing assays. Dual-luciferase reporter and RNA pull-down assays were applied to validate the interaction among NR2F1-AS1, miR-493-5p and GOLM1. Furthermore, in vivo experiments were conducted to demonstrate the oncogenic role of NR2F1-AS1 in melanoma.
Up-regulated NR2F1-AS1 and down-regulated miR-493-5p were detected in melanoma tumors and cells. The overexpression of NR2F1-AS1 was induced by STAT3. High NR2F1-AS1 expression was correlated to advanced tumor stage and poor prognosis of melanoma. Functional studies using CCK-8, Edu, transwell and wound healing assays revealed that the proliferative, migratory and invasive capacities of melanoma cells were attenuated by the by inhibition of NR2F1-AS1. Moreover, NR2F1-AS1 was able to up-regulate GOLM1 through recognizing and binding miR-493-5p. Furthermore, knockdown of miR-493-5p distinctly reversed these inhibitory effects of NR2F1-AS1 down-regulation on the tumorigenesis and progression of melanoma.
Our findings demonstrate a key role for NR2F1-AS1 in melanoma progression via targeting miR-493-5p/GOLM1 axis.</description><subject>Antisense RNA</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Cholecystokinin</subject><subject>Chromatin</subject><subject>COUP Transcription Factor I - genetics</subject><subject>COUP Transcription Factor I - metabolism</subject><subject>Disease Progression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene therapy</subject><subject>Humans</subject><subject>Immunoprecipitation</subject><subject>Melanoma</subject><subject>Melanoma - genetics</subject><subject>Melanoma - metabolism</subject><subject>Membrane Proteins - metabolism</subject><subject>MicroRNAs - metabolism</subject><subject>Non-coding RNA</subject><subject>Polymerase chain reaction</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>Signal Transduction</subject><subject>Stat3 protein</subject><subject>STAT3 Transcription Factor - genetics</subject><subject>Transcription</subject><subject>Tumorigenesis</subject><subject>Wound healing</subject><issn>1099-498X</issn><issn>1521-2254</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkc1KAzEUhYMoWn_AJ5CAGzdjb_5mJssiVoWqUCu4G9KZTE2ZmdQkU_QBfG-jVgVX9yy-e_jgIHRM4JwA0OFy0Z4zxvItNCCCkoRSwbdjBikTLvOnPbTv_RKAZHkud9FeRCnlHAbo_WE2mjGsymDWKmiPw7PGwanOl86sgrEdtjVuunJ6N8J3UzomyeiB4GDxytnWBv31EPPCae83eKsb1dlW4bVR2OlF36hgusUX2pppVGKJWA2v7ie3BKtX4w_RTq0ar4829wA9ji9nF9fJ5P7q5mI0SUpGSEhkJqmiFaSKVBWrGagyBz7PCKNci6wioqZM1JBpIFKB4JAyVqVQs5rOFdfsAJ1990bhl177ULTGl7qJutr2vqACJE0zyERET_-hS9u7LtpFiuc8lZCKv8LSWe-drouVM61ybwWB4nOaIk5TfE4T0ZNNYT9vdfUL_mzBPgC4H4Z1</recordid><startdate>202107</startdate><enddate>202107</enddate><creator>Bai, Mei</creator><creator>Wu, Zong-Zhou</creator><creator>Huang, Yan-Li</creator><creator>Ke, Jin</creator><creator>Xu, Qing</creator><creator>Wang, Xiong</creator><general>Wiley Periodicals Inc</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>7QP</scope><scope>7TK</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-9778-7377</orcidid></search><sort><creationdate>202107</creationdate><title>STAT3 activates the transcription of lncRNA NR2F1-AS1 to promote the progression of melanoma via regulating the miR-493-5p/GOLM1 axis</title><author>Bai, Mei ; Wu, Zong-Zhou ; Huang, Yan-Li ; Ke, Jin ; Xu, Qing ; Wang, Xiong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c311t-9792a2d06a1dd3f30ac804b71324e57d15f235f07e019a0540633d60f3f2ba4e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Antisense RNA</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Cholecystokinin</topic><topic>Chromatin</topic><topic>COUP Transcription Factor I - genetics</topic><topic>COUP Transcription Factor I - metabolism</topic><topic>Disease Progression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene therapy</topic><topic>Humans</topic><topic>Immunoprecipitation</topic><topic>Melanoma</topic><topic>Melanoma - genetics</topic><topic>Melanoma - metabolism</topic><topic>Membrane Proteins - metabolism</topic><topic>MicroRNAs - metabolism</topic><topic>Non-coding RNA</topic><topic>Polymerase chain reaction</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>Signal Transduction</topic><topic>Stat3 protein</topic><topic>STAT3 Transcription Factor - genetics</topic><topic>Transcription</topic><topic>Tumorigenesis</topic><topic>Wound healing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bai, Mei</creatorcontrib><creatorcontrib>Wu, Zong-Zhou</creatorcontrib><creatorcontrib>Huang, Yan-Li</creatorcontrib><creatorcontrib>Ke, Jin</creatorcontrib><creatorcontrib>Xu, Qing</creatorcontrib><creatorcontrib>Wang, Xiong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The journal of gene medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bai, Mei</au><au>Wu, Zong-Zhou</au><au>Huang, Yan-Li</au><au>Ke, Jin</au><au>Xu, Qing</au><au>Wang, Xiong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>STAT3 activates the transcription of lncRNA NR2F1-AS1 to promote the progression of melanoma via regulating the miR-493-5p/GOLM1 axis</atitle><jtitle>The journal of gene medicine</jtitle><addtitle>J Gene Med</addtitle><date>2021-07</date><risdate>2021</risdate><volume>23</volume><issue>7</issue><spage>e3338</spage><epage>e3338</epage><pages>e3338-e3338</pages><issn>1099-498X</issn><eissn>1521-2254</eissn><abstract>Long non-coding RNAs (lncRNAs) are vital regulators during the biological processes of melanoma. The present study aimed to uncover biological functions of lncRNA termed NR2F1 antisense RNA 1 (NR2F1-AS1) in melanoma and the potential mechanisms.
Relative levels of NR2F1-AS1 and miR-493-5p in a total of 137 paired primary melanoma tissues and corresponding non-tumor tissues, as well as three melanoma cell lines, were examined by a real-time polymerase chain reaction. The clinical significance of NR2F1-AS1 expression was analyzed statistically. The STAT3 binding motif in the promoter region of NR2F1-AS1 was identified by JASPAR (http://jaspar.genereg.net). The association between STAT3 and NR2F1-AS1 was determined by dual-luciferase reporter and chromatin immunoprecipitation assays. The effects of NR2F1-AS1 on cell proliferation, migration and were measured by cell counting kit-8 (CCK-8), Edu, transwell and wound healing assays. Dual-luciferase reporter and RNA pull-down assays were applied to validate the interaction among NR2F1-AS1, miR-493-5p and GOLM1. Furthermore, in vivo experiments were conducted to demonstrate the oncogenic role of NR2F1-AS1 in melanoma.
Up-regulated NR2F1-AS1 and down-regulated miR-493-5p were detected in melanoma tumors and cells. The overexpression of NR2F1-AS1 was induced by STAT3. High NR2F1-AS1 expression was correlated to advanced tumor stage and poor prognosis of melanoma. Functional studies using CCK-8, Edu, transwell and wound healing assays revealed that the proliferative, migratory and invasive capacities of melanoma cells were attenuated by the by inhibition of NR2F1-AS1. Moreover, NR2F1-AS1 was able to up-regulate GOLM1 through recognizing and binding miR-493-5p. Furthermore, knockdown of miR-493-5p distinctly reversed these inhibitory effects of NR2F1-AS1 down-regulation on the tumorigenesis and progression of melanoma.
Our findings demonstrate a key role for NR2F1-AS1 in melanoma progression via targeting miR-493-5p/GOLM1 axis.</abstract><cop>England</cop><pub>Wiley Periodicals Inc</pub><pmid>33822440</pmid><doi>10.1002/jgm.3338</doi><orcidid>https://orcid.org/0000-0002-9778-7377</orcidid></addata></record> |
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| subjects | Antisense RNA Cell Line, Tumor Cell migration Cell Movement Cell Proliferation Cholecystokinin Chromatin COUP Transcription Factor I - genetics COUP Transcription Factor I - metabolism Disease Progression Gene Expression Regulation, Neoplastic Gene therapy Humans Immunoprecipitation Melanoma Melanoma - genetics Melanoma - metabolism Membrane Proteins - metabolism MicroRNAs - metabolism Non-coding RNA Polymerase chain reaction RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Signal Transduction Stat3 protein STAT3 Transcription Factor - genetics Transcription Tumorigenesis Wound healing |
| title | STAT3 activates the transcription of lncRNA NR2F1-AS1 to promote the progression of melanoma via regulating the miR-493-5p/GOLM1 axis |
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