Long noncoding RNA LINC01291 promotes the aggressive properties of melanoma by functioning as a competing endogenous RNA for microRNA-625-5p and subsequently increasing IGF-1R expression
Studies have confirmed the relationship between dysregulated long noncoding RNAs and melanoma pathogenesis. However, the regulatory functions of long intergenic non-protein coding RNA 1291 (LINC01291) in melanoma remain unknown. Therefore, we evaluated LINC01291 expression in melanoma and explored i...
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| Veröffentlicht in: | Cancer gene therapy 2022-03, Vol.29 (3-4), p.341-357 |
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| creator | Wu, Lijun Li, Ke Lin, Wei Liu, Jianjiang Qi, Qiang Shen, Guoliang Chen, Weixin He, Wenjun |
| description | Studies have confirmed the relationship between dysregulated long noncoding RNAs and melanoma pathogenesis. However, the regulatory functions of long intergenic non-protein coding RNA 1291 (LINC01291) in melanoma remain unknown. Therefore, we evaluated LINC01291 expression in melanoma and explored its roles in regulating tumor behaviors. Further, the molecular events via which LINC01291 affects melanoma cells were investigated. LINC01291 expression in melanoma cells was analyzed using The Cancer Genome Atlas database and quantitative real-time polymerase chain reaction. Functional assays, including the Cell Counting Kit-8 assay, colony formation assay, flow cytometry, cell migration and invasion assays, and tumor xenograft models, were used to examine LINC01291’s role in melanoma cells. Additionally, bioinformatics analysis, RNA immunoprecipitation, luciferase reporter assay, and western blotting were conducted to determine the tumor-promoting mechanism of LINC01291. LINC01291 was upregulated in melanoma tissues and cell lines. Following LINC01291 knockdown, cell proliferation, colony formation, migration, and invasion were diminished, whereas apoptosis was enhanced and the cell cycle was arrested at G0/G1. In addition, loss of LINC01291 decreased the chemoresistance of melanoma cells to cisplatin. Furthermore, LINC01291 interference inhibited melanoma tumor growth in vivo. Mechanistically, LINC01291 functions as a competing endogenous RNA by sponging microRNA-625-5p (miR-625-5p) in melanoma cells and maintaining insulin-like growth factor 1 receptor (IGF-1R) expression. Rescue experiments revealed that the roles induced by LINC01291 depletion in melanoma cells could be reversed by suppressing miR-625-5p or overexpressing IGF-1R. Our study identified the LINC01291/miR-625-5p/IGF-1R competing endogenous RNA pathway in melanoma cells, which may represent a novel diagnostic biomarker and an effective therapeutic target for melanoma. |
| doi_str_mv | 10.1038/s41417-021-00313-9 |
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However, the regulatory functions of long intergenic non-protein coding RNA 1291 (LINC01291) in melanoma remain unknown. Therefore, we evaluated LINC01291 expression in melanoma and explored its roles in regulating tumor behaviors. Further, the molecular events via which LINC01291 affects melanoma cells were investigated. LINC01291 expression in melanoma cells was analyzed using The Cancer Genome Atlas database and quantitative real-time polymerase chain reaction. Functional assays, including the Cell Counting Kit-8 assay, colony formation assay, flow cytometry, cell migration and invasion assays, and tumor xenograft models, were used to examine LINC01291’s role in melanoma cells. Additionally, bioinformatics analysis, RNA immunoprecipitation, luciferase reporter assay, and western blotting were conducted to determine the tumor-promoting mechanism of LINC01291. LINC01291 was upregulated in melanoma tissues and cell lines. Following LINC01291 knockdown, cell proliferation, colony formation, migration, and invasion were diminished, whereas apoptosis was enhanced and the cell cycle was arrested at G0/G1. In addition, loss of LINC01291 decreased the chemoresistance of melanoma cells to cisplatin. Furthermore, LINC01291 interference inhibited melanoma tumor growth in vivo. Mechanistically, LINC01291 functions as a competing endogenous RNA by sponging microRNA-625-5p (miR-625-5p) in melanoma cells and maintaining insulin-like growth factor 1 receptor (IGF-1R) expression. Rescue experiments revealed that the roles induced by LINC01291 depletion in melanoma cells could be reversed by suppressing miR-625-5p or overexpressing IGF-1R. Our study identified the LINC01291/miR-625-5p/IGF-1R competing endogenous RNA pathway in melanoma cells, which may represent a novel diagnostic biomarker and an effective therapeutic target for melanoma.</description><identifier>ISSN: 0929-1903</identifier><identifier>EISSN: 1476-5500</identifier><identifier>DOI: 10.1038/s41417-021-00313-9</identifier><identifier>PMID: 33674778</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>13/95 ; 38/77 ; 42/109 ; 42/89 ; 631/67/1813/1634 ; 631/80 ; 64/60 ; 82/80 ; 96/2 ; 96/31 ; Apoptosis ; Bioinformatics ; Biomedical and Life Sciences ; Biomedicine ; Cell cycle ; Cell Line, Tumor ; Cell migration ; Cell Movement - genetics ; Cell proliferation ; Cell Proliferation - genetics ; Chemoresistance ; Cisplatin ; Colonies ; Flow cytometry ; Gene Expression ; Gene Expression Regulation, Neoplastic ; Gene Therapy ; Genomes ; Humans ; Immunoprecipitation ; Insulin ; Insulin-like growth factors ; Melanoma ; Melanoma - genetics ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; Polymerase chain reaction ; Receptor, IGF Type 1 - metabolism ; Ribonucleic acid ; RNA ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; Therapeutic targets ; Tumors ; Western blotting ; Xenografts</subject><ispartof>Cancer gene therapy, 2022-03, Vol.29 (3-4), p.341-357</ispartof><rights>The Author(s), under exclusive licence to Springer Nature America, Inc. part of Springer Nature 2021</rights><rights>2021. The Author(s), under exclusive licence to Springer Nature America, Inc. part of Springer Nature.</rights><rights>The Author(s), under exclusive licence to Springer Nature America, Inc. part of Springer Nature 2021. 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-c540t-7e8717029ee986050e70497cd2b44d7995663d6f979955fc30f19e9eee39dbac3</citedby><cites>FETCH-LOGICAL-c540t-7e8717029ee986050e70497cd2b44d7995663d6f979955fc30f19e9eee39dbac3</cites><orcidid>0000-0002-4873-3495</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/s41417-021-00313-9$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/s41417-021-00313-9$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,777,781,882,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33674778$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Lijun</creatorcontrib><creatorcontrib>Li, Ke</creatorcontrib><creatorcontrib>Lin, Wei</creatorcontrib><creatorcontrib>Liu, Jianjiang</creatorcontrib><creatorcontrib>Qi, Qiang</creatorcontrib><creatorcontrib>Shen, Guoliang</creatorcontrib><creatorcontrib>Chen, Weixin</creatorcontrib><creatorcontrib>He, Wenjun</creatorcontrib><title>Long noncoding RNA LINC01291 promotes the aggressive properties of melanoma by functioning as a competing endogenous RNA for microRNA-625-5p and subsequently increasing IGF-1R expression</title><title>Cancer gene therapy</title><addtitle>Cancer Gene Ther</addtitle><addtitle>Cancer Gene Ther</addtitle><description>Studies have confirmed the relationship between dysregulated long noncoding RNAs and melanoma pathogenesis. However, the regulatory functions of long intergenic non-protein coding RNA 1291 (LINC01291) in melanoma remain unknown. Therefore, we evaluated LINC01291 expression in melanoma and explored its roles in regulating tumor behaviors. Further, the molecular events via which LINC01291 affects melanoma cells were investigated. LINC01291 expression in melanoma cells was analyzed using The Cancer Genome Atlas database and quantitative real-time polymerase chain reaction. Functional assays, including the Cell Counting Kit-8 assay, colony formation assay, flow cytometry, cell migration and invasion assays, and tumor xenograft models, were used to examine LINC01291’s role in melanoma cells. Additionally, bioinformatics analysis, RNA immunoprecipitation, luciferase reporter assay, and western blotting were conducted to determine the tumor-promoting mechanism of LINC01291. LINC01291 was upregulated in melanoma tissues and cell lines. Following LINC01291 knockdown, cell proliferation, colony formation, migration, and invasion were diminished, whereas apoptosis was enhanced and the cell cycle was arrested at G0/G1. In addition, loss of LINC01291 decreased the chemoresistance of melanoma cells to cisplatin. Furthermore, LINC01291 interference inhibited melanoma tumor growth in vivo. Mechanistically, LINC01291 functions as a competing endogenous RNA by sponging microRNA-625-5p (miR-625-5p) in melanoma cells and maintaining insulin-like growth factor 1 receptor (IGF-1R) expression. Rescue experiments revealed that the roles induced by LINC01291 depletion in melanoma cells could be reversed by suppressing miR-625-5p or overexpressing IGF-1R. Our study identified the LINC01291/miR-625-5p/IGF-1R competing endogenous RNA pathway in melanoma cells, which may represent a novel diagnostic biomarker and an effective therapeutic target for melanoma.</description><subject>13/95</subject><subject>38/77</subject><subject>42/109</subject><subject>42/89</subject><subject>631/67/1813/1634</subject><subject>631/80</subject><subject>64/60</subject><subject>82/80</subject><subject>96/2</subject><subject>96/31</subject><subject>Apoptosis</subject><subject>Bioinformatics</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell cycle</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement - genetics</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - genetics</subject><subject>Chemoresistance</subject><subject>Cisplatin</subject><subject>Colonies</subject><subject>Flow cytometry</subject><subject>Gene Expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene Therapy</subject><subject>Genomes</subject><subject>Humans</subject><subject>Immunoprecipitation</subject><subject>Insulin</subject><subject>Insulin-like growth factors</subject><subject>Melanoma</subject><subject>Melanoma - genetics</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Polymerase chain reaction</subject><subject>Receptor, IGF Type 1 - metabolism</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>Therapeutic targets</subject><subject>Tumors</subject><subject>Western blotting</subject><subject>Xenografts</subject><issn>0929-1903</issn><issn>1476-5500</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>C6C</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>eNp9Ustu1DAUjRCITgs_wAJZYsPG4FfieINUjWg70qhIFawtx7lJXU3sYCdV59f4OpyZUh4LVr72Offch09RvKHkAyW8_pgEFVRiwigmhFOO1bNiRYWscFkS8rxYEcUUporwk-I0pTtCMij5y-KE80rmsF4VP7bB98gHb0PrcnRzfY62m-s1oUxRNMYwhAkSmm4Bmb6PkJK7h-V9hDi5jIQODbAzPgwGNXvUzd5OLvhFyyRkkA3DCNNyBd-GHnyY06FKFyIanI0hX3DFSlyOyPgWpblJ8H0GP-32yHkbwaQlfXN5gekNgofx0EXwr4oXndkleP14nhXfLj5_XV_h7ZfLzfp8i20pyIQl1JJKwhSAqitSEpBEKGlb1gjRSqXKquJt1aklLDvLSUcVZDZw1TbG8rPi01F3nJsBWps7i2anx-gGE_c6GKf_Rry71X2417USpGIsC7x_FIghD5YmPbhkYZe3BnkbmglVi5pLRTP13T_UuzBHn8fTrMqfLfIciyA7svL2UorQPTVDiV6soY_W0Nka-mANrXLS2z_HeEr55YVM4EdCypDvIf6u_R_Zn1Fjxf0</recordid><startdate>20220301</startdate><enddate>20220301</enddate><creator>Wu, Lijun</creator><creator>Li, Ke</creator><creator>Lin, Wei</creator><creator>Liu, Jianjiang</creator><creator>Qi, Qiang</creator><creator>Shen, Guoliang</creator><creator>Chen, Weixin</creator><creator>He, Wenjun</creator><general>Nature Publishing Group US</general><general>Nature Publishing Group</general><scope>C6C</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>7QP</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</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>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>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-4873-3495</orcidid></search><sort><creationdate>20220301</creationdate><title>Long noncoding RNA LINC01291 promotes the aggressive properties of melanoma by functioning as a competing endogenous RNA for microRNA-625-5p and subsequently increasing IGF-1R expression</title><author>Wu, Lijun ; Li, Ke ; Lin, Wei ; Liu, Jianjiang ; Qi, Qiang ; Shen, Guoliang ; Chen, Weixin ; He, Wenjun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c540t-7e8717029ee986050e70497cd2b44d7995663d6f979955fc30f19e9eee39dbac3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>13/95</topic><topic>38/77</topic><topic>42/109</topic><topic>42/89</topic><topic>631/67/1813/1634</topic><topic>631/80</topic><topic>64/60</topic><topic>82/80</topic><topic>96/2</topic><topic>96/31</topic><topic>Apoptosis</topic><topic>Bioinformatics</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell cycle</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell Movement - genetics</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - genetics</topic><topic>Chemoresistance</topic><topic>Cisplatin</topic><topic>Colonies</topic><topic>Flow cytometry</topic><topic>Gene Expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene Therapy</topic><topic>Genomes</topic><topic>Humans</topic><topic>Immunoprecipitation</topic><topic>Insulin</topic><topic>Insulin-like growth factors</topic><topic>Melanoma</topic><topic>Melanoma - genetics</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miRNA</topic><topic>Polymerase chain reaction</topic><topic>Receptor, IGF Type 1 - metabolism</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>Therapeutic targets</topic><topic>Tumors</topic><topic>Western blotting</topic><topic>Xenografts</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Lijun</creatorcontrib><creatorcontrib>Li, Ke</creatorcontrib><creatorcontrib>Lin, Wei</creatorcontrib><creatorcontrib>Liu, Jianjiang</creatorcontrib><creatorcontrib>Qi, Qiang</creatorcontrib><creatorcontrib>Shen, Guoliang</creatorcontrib><creatorcontrib>Chen, Weixin</creatorcontrib><creatorcontrib>He, Wenjun</creatorcontrib><collection>Springer Nature OA/Free Journals</collection><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>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</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 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>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>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer gene therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Lijun</au><au>Li, Ke</au><au>Lin, Wei</au><au>Liu, Jianjiang</au><au>Qi, Qiang</au><au>Shen, Guoliang</au><au>Chen, Weixin</au><au>He, Wenjun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Long noncoding RNA LINC01291 promotes the aggressive properties of melanoma by functioning as a competing endogenous RNA for microRNA-625-5p and subsequently increasing IGF-1R expression</atitle><jtitle>Cancer gene therapy</jtitle><stitle>Cancer Gene Ther</stitle><addtitle>Cancer Gene Ther</addtitle><date>2022-03-01</date><risdate>2022</risdate><volume>29</volume><issue>3-4</issue><spage>341</spage><epage>357</epage><pages>341-357</pages><issn>0929-1903</issn><eissn>1476-5500</eissn><abstract>Studies have confirmed the relationship between dysregulated long noncoding RNAs and melanoma pathogenesis. However, the regulatory functions of long intergenic non-protein coding RNA 1291 (LINC01291) in melanoma remain unknown. Therefore, we evaluated LINC01291 expression in melanoma and explored its roles in regulating tumor behaviors. Further, the molecular events via which LINC01291 affects melanoma cells were investigated. LINC01291 expression in melanoma cells was analyzed using The Cancer Genome Atlas database and quantitative real-time polymerase chain reaction. Functional assays, including the Cell Counting Kit-8 assay, colony formation assay, flow cytometry, cell migration and invasion assays, and tumor xenograft models, were used to examine LINC01291’s role in melanoma cells. Additionally, bioinformatics analysis, RNA immunoprecipitation, luciferase reporter assay, and western blotting were conducted to determine the tumor-promoting mechanism of LINC01291. LINC01291 was upregulated in melanoma tissues and cell lines. Following LINC01291 knockdown, cell proliferation, colony formation, migration, and invasion were diminished, whereas apoptosis was enhanced and the cell cycle was arrested at G0/G1. In addition, loss of LINC01291 decreased the chemoresistance of melanoma cells to cisplatin. Furthermore, LINC01291 interference inhibited melanoma tumor growth in vivo. Mechanistically, LINC01291 functions as a competing endogenous RNA by sponging microRNA-625-5p (miR-625-5p) in melanoma cells and maintaining insulin-like growth factor 1 receptor (IGF-1R) expression. Rescue experiments revealed that the roles induced by LINC01291 depletion in melanoma cells could be reversed by suppressing miR-625-5p or overexpressing IGF-1R. Our study identified the LINC01291/miR-625-5p/IGF-1R competing endogenous RNA pathway in melanoma cells, which may represent a novel diagnostic biomarker and an effective therapeutic target for melanoma.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>33674778</pmid><doi>10.1038/s41417-021-00313-9</doi><tpages>17</tpages><orcidid>https://orcid.org/0000-0002-4873-3495</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 13/95 38/77 42/109 42/89 631/67/1813/1634 631/80 64/60 82/80 96/2 96/31 Apoptosis Bioinformatics Biomedical and Life Sciences Biomedicine Cell cycle Cell Line, Tumor Cell migration Cell Movement - genetics Cell proliferation Cell Proliferation - genetics Chemoresistance Cisplatin Colonies Flow cytometry Gene Expression Gene Expression Regulation, Neoplastic Gene Therapy Genomes Humans Immunoprecipitation Insulin Insulin-like growth factors Melanoma Melanoma - genetics MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism miRNA Polymerase chain reaction Receptor, IGF Type 1 - metabolism Ribonucleic acid RNA RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Therapeutic targets Tumors Western blotting Xenografts |
| title | Long noncoding RNA LINC01291 promotes the aggressive properties of melanoma by functioning as a competing endogenous RNA for microRNA-625-5p and subsequently increasing IGF-1R expression |
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