Gene expression profiling after LINC00472 overexpression in an NSCLC cell line1
Lung cancer accounts for a large proportion of cancer-related deaths worldwide. Personalized therapeutic medicine based on the genetic characteristics of non-small cell lung cancer (NSCLC) is a promising field, and discovering clinically applicable biomarkers of NSCLC is required. LINC00472 is a lon...
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| Veröffentlicht in: | Cancer biomarkers : section A of Disease markers 2021, Vol.32 (2), p.175-188 |
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| creator | Seo, Danbi Roh, Jungwook Chae, Yeonsoo Kim, Wanyeon |
| description | Lung cancer accounts for a large proportion of cancer-related deaths worldwide. Personalized therapeutic medicine based on the genetic characteristics of non-small cell lung cancer (NSCLC) is a promising field, and discovering clinically applicable biomarkers of NSCLC is required. LINC00472 is a long non-coding RNA and has been recently suggested to be a biomarker of NSCLC, but little is known of its mechanism in NSCLC. Thus, the current study was performed to document changes in gene expression after LINC00472 overexpression in NSCLC cells. As a result of cell viability and migration assay, LINC00472 downregulated cell survival, proliferation, and motility. Transcriptome sequencing analysis showed 3,782 genes expression were changed in LINC00472 overexpressing cells. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis showed most genes were associated with intracellular metabolism. The PPP1R12B, RGS5, RBM5, RBL2, LDLR and PTPRM genes were upregulated by LINC00472 overexpression and these genes functioned as tumor suppressors in several cancers. In contrast, SPSB1, PCNA, CD24, CDK5, CDC25A, and EIF4EBP1 were downregulated by LINC00472, and they functioned as oncogenes in various cancers. Consequently, the function of LINC00472 in tumorigenesis might be related to changes in the expressions of other oncogenes and tumor suppressors. |
| doi_str_mv | 10.3233/CBM-210242 |
| format | Article |
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Personalized therapeutic medicine based on the genetic characteristics of non-small cell lung cancer (NSCLC) is a promising field, and discovering clinically applicable biomarkers of NSCLC is required. LINC00472 is a long non-coding RNA and has been recently suggested to be a biomarker of NSCLC, but little is known of its mechanism in NSCLC. Thus, the current study was performed to document changes in gene expression after LINC00472 overexpression in NSCLC cells. As a result of cell viability and migration assay, LINC00472 downregulated cell survival, proliferation, and motility. Transcriptome sequencing analysis showed 3,782 genes expression were changed in LINC00472 overexpressing cells. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis showed most genes were associated with intracellular metabolism. The PPP1R12B, RGS5, RBM5, RBL2, LDLR and PTPRM genes were upregulated by LINC00472 overexpression and these genes functioned as tumor suppressors in several cancers. In contrast, SPSB1, PCNA, CD24, CDK5, CDC25A, and EIF4EBP1 were downregulated by LINC00472, and they functioned as oncogenes in various cancers. 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Personalized therapeutic medicine based on the genetic characteristics of non-small cell lung cancer (NSCLC) is a promising field, and discovering clinically applicable biomarkers of NSCLC is required. LINC00472 is a long non-coding RNA and has been recently suggested to be a biomarker of NSCLC, but little is known of its mechanism in NSCLC. Thus, the current study was performed to document changes in gene expression after LINC00472 overexpression in NSCLC cells. As a result of cell viability and migration assay, LINC00472 downregulated cell survival, proliferation, and motility. Transcriptome sequencing analysis showed 3,782 genes expression were changed in LINC00472 overexpressing cells. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis showed most genes were associated with intracellular metabolism. The PPP1R12B, RGS5, RBM5, RBL2, LDLR and PTPRM genes were upregulated by LINC00472 overexpression and these genes functioned as tumor suppressors in several cancers. In contrast, SPSB1, PCNA, CD24, CDK5, CDC25A, and EIF4EBP1 were downregulated by LINC00472, and they functioned as oncogenes in various cancers. Consequently, the function of LINC00472 in tumorigenesis might be related to changes in the expressions of other oncogenes and tumor suppressors.</description><subject>Carcinogenesis - genetics</subject><subject>Carcinoma, Non-Small-Cell Lung - genetics</subject><subject>Carcinoma, Non-Small-Cell Lung - pathology</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - genetics</subject><subject>Cell Proliferation - genetics</subject><subject>Cell Survival - genetics</subject><subject>Down-Regulation</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - pathology</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>RNA-Seq</subject><subject>Up-Regulation</subject><issn>1574-0153</issn><issn>1875-8592</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkD1PwzAURS0EoqWw8AOQR4QU8GccjxBBqRTaAZgj23lGQWlS7BbBv8dVC2J6bzj36uogdE7JNWec35R3TxmjhAl2gMa0UDIrpGaH6ZdKZIRKPkInMb4TIjhl-hiNuOBaCSLHaDGFHjB8rQLE2A49XoXBt13bv2Hj1xBwNZuXKagYHj4h_APbHpsez5_LqsQOug6nENBTdORNF-Fsfyfo9eH-pXzMqsV0Vt5WmaOcySx31BuwTjoncnC5UBS0zx1TObUAXFvvlXHS68Y2jS2I1UJ4lktXJMgyPkGXu96092MDcV0v27idYXoYNrFmMqeapVqe0Ksd6sIQYwBfr0K7NOG7pqTeCqyTwHonMMEX-96NXULzh_4a4z-TMmnx</recordid><startdate>2021</startdate><enddate>2021</enddate><creator>Seo, Danbi</creator><creator>Roh, Jungwook</creator><creator>Chae, Yeonsoo</creator><creator>Kim, Wanyeon</creator><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>7X8</scope></search><sort><creationdate>2021</creationdate><title>Gene expression profiling after LINC00472 overexpression in an NSCLC cell line1</title><author>Seo, Danbi ; Roh, Jungwook ; Chae, Yeonsoo ; Kim, Wanyeon</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c1325-6c1faebc5cc46ec6471e9f6c2761bee39bff7ac5f9dbddb80b944f265c86c2b23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Carcinogenesis - genetics</topic><topic>Carcinoma, Non-Small-Cell Lung - genetics</topic><topic>Carcinoma, Non-Small-Cell Lung - pathology</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - genetics</topic><topic>Cell Proliferation - genetics</topic><topic>Cell Survival - genetics</topic><topic>Down-Regulation</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - pathology</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>RNA-Seq</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Seo, Danbi</creatorcontrib><creatorcontrib>Roh, Jungwook</creatorcontrib><creatorcontrib>Chae, Yeonsoo</creatorcontrib><creatorcontrib>Kim, Wanyeon</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer biomarkers : section A of Disease markers</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Seo, Danbi</au><au>Roh, Jungwook</au><au>Chae, Yeonsoo</au><au>Kim, Wanyeon</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Gene expression profiling after LINC00472 overexpression in an NSCLC cell line1</atitle><jtitle>Cancer biomarkers : section A of Disease markers</jtitle><addtitle>Cancer Biomark</addtitle><date>2021</date><risdate>2021</risdate><volume>32</volume><issue>2</issue><spage>175</spage><epage>188</epage><pages>175-188</pages><issn>1574-0153</issn><eissn>1875-8592</eissn><abstract>Lung cancer accounts for a large proportion of cancer-related deaths worldwide. 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| subjects | Carcinogenesis - genetics Carcinoma, Non-Small-Cell Lung - genetics Carcinoma, Non-Small-Cell Lung - pathology Cell Line, Tumor Cell Movement - genetics Cell Proliferation - genetics Cell Survival - genetics Down-Regulation Gene Expression Profiling Gene Expression Regulation, Neoplastic Humans Lung Neoplasms - genetics Lung Neoplasms - pathology RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism RNA-Seq Up-Regulation |
| title | Gene expression profiling after LINC00472 overexpression in an NSCLC cell line1 |
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