Identify CTBP1-DT as an immunological biomarker that promotes lipid synthesis and apoptosis resistance in KIRC

•CTBP1-DT is a lncRNA located in the nucleus that is significantly upregulated in clear cell renal cell carcinoma.•Downregulate CTBP1-DT could inhibit cell lipid content.•CTBP1-DT is linked with immune cell infiltration in clear cell renal cell carcinoma, especially macrophages. Recently, mounting e...

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Veröffentlicht in:Gene 2024-07, Vol.914, p.148403-148403, Article 148403
Hauptverfasser: Li, Haolin, Fei, Mintian, Zhang, Yi, Xu, Qili, Feng, Rui, Cao, Jing, Qu, Yan, Xiao, Haibing
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container_start_page 148403
container_title Gene
container_volume 914
creator Li, Haolin
Fei, Mintian
Zhang, Yi
Xu, Qili
Feng, Rui
Cao, Jing
Qu, Yan
Xiao, Haibing
description •CTBP1-DT is a lncRNA located in the nucleus that is significantly upregulated in clear cell renal cell carcinoma.•Downregulate CTBP1-DT could inhibit cell lipid content.•CTBP1-DT is linked with immune cell infiltration in clear cell renal cell carcinoma, especially macrophages. Recently, mounting evidence has highlighted the essential function of the C-terminal binding protein-1 divergent transcript (CTBP1-DT) in malignancies. However, its role in kidney renal clear cell carcinoma (KIRC) remains largely unknown. Our study aimed to identify the potential function of CTBP1-DT in KIRC. RT-qPCR, Kaplan-Meier survival analysis, Cox regression analysis, and nomogram analysis were utilized to determine the expression and effects of CTBP1-DT on survival. The subcellular localization of CTBP1-DT was determined using RNA fluorescence in situ hybridization (FISH). To investigate the functions of CTBP1-DT in regulating KIRC cell proliferation, migration, invasion, lipid synthesis, and apoptosis, we conducted CCK8, EdU, Transwell, and Oil Red O staining and cell apoptosis staining assays. The relationships between CTBP1-DT and the tumor microenvironment were investigated with multiple bioinformatics analysis algorithms and databases, including CYBERSORT, TIMER2, Spearman correlation test, tumor mutation burden (TMB), microsatellite instability (MSI), and immunophenoscore (IPS). According to our results, CTBP1-DT is a lncRNA located in the nucleus that is significantly upregulated in KIRC and is correlated with better clinical outcomes. Downregulating CTBP1-DT inhibited cell viability, migration, invasion, and lipid synthesis but triggered cell apoptosis. Additionally, we explored the potential effect of CTBP1-DT in regulating immune cell infiltration in KIRC and other malignancies. Furthermore, CTBP1-DT could be used to predict the effectiveness of targeted drugs and immune checkpoint inhibitors. In conclusion, we identified CTBP1-DT as a potential immunological biomarker and discovered the potential role of CTBP1-DT in regulating lipid synthesis and apoptosis resistance.
doi_str_mv 10.1016/j.gene.2024.148403
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Recently, mounting evidence has highlighted the essential function of the C-terminal binding protein-1 divergent transcript (CTBP1-DT) in malignancies. However, its role in kidney renal clear cell carcinoma (KIRC) remains largely unknown. Our study aimed to identify the potential function of CTBP1-DT in KIRC. RT-qPCR, Kaplan-Meier survival analysis, Cox regression analysis, and nomogram analysis were utilized to determine the expression and effects of CTBP1-DT on survival. The subcellular localization of CTBP1-DT was determined using RNA fluorescence in situ hybridization (FISH). To investigate the functions of CTBP1-DT in regulating KIRC cell proliferation, migration, invasion, lipid synthesis, and apoptosis, we conducted CCK8, EdU, Transwell, and Oil Red O staining and cell apoptosis staining assays. The relationships between CTBP1-DT and the tumor microenvironment were investigated with multiple bioinformatics analysis algorithms and databases, including CYBERSORT, TIMER2, Spearman correlation test, tumor mutation burden (TMB), microsatellite instability (MSI), and immunophenoscore (IPS). According to our results, CTBP1-DT is a lncRNA located in the nucleus that is significantly upregulated in KIRC and is correlated with better clinical outcomes. Downregulating CTBP1-DT inhibited cell viability, migration, invasion, and lipid synthesis but triggered cell apoptosis. Additionally, we explored the potential effect of CTBP1-DT in regulating immune cell infiltration in KIRC and other malignancies. Furthermore, CTBP1-DT could be used to predict the effectiveness of targeted drugs and immune checkpoint inhibitors. In conclusion, we identified CTBP1-DT as a potential immunological biomarker and discovered the potential role of CTBP1-DT in regulating lipid synthesis and apoptosis resistance.</description><identifier>ISSN: 0378-1119</identifier><identifier>EISSN: 1879-0038</identifier><identifier>DOI: 10.1016/j.gene.2024.148403</identifier><identifier>PMID: 38521112</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Alcohol Oxidoreductases - genetics ; Alcohol Oxidoreductases - metabolism ; Apoptosis ; Biomarkers, Tumor - genetics ; Biomarkers, Tumor - metabolism ; Carcinoma, Renal Cell - genetics ; Carcinoma, Renal Cell - immunology ; Carcinoma, Renal Cell - metabolism ; Carcinoma, Renal Cell - pathology ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; CTBP1-DT ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Kidney Neoplasms - genetics ; Kidney Neoplasms - immunology ; Kidney Neoplasms - metabolism ; Kidney Neoplasms - pathology ; KIRC ; Lipid ; Lipids ; lncRNA ; Male ; Prognosis ; RNA, Long Noncoding - genetics ; Tumor Microenvironment</subject><ispartof>Gene, 2024-07, Vol.914, p.148403-148403, Article 148403</ispartof><rights>2024 Elsevier B.V.</rights><rights>Copyright © 2024 Elsevier B.V. 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Recently, mounting evidence has highlighted the essential function of the C-terminal binding protein-1 divergent transcript (CTBP1-DT) in malignancies. However, its role in kidney renal clear cell carcinoma (KIRC) remains largely unknown. Our study aimed to identify the potential function of CTBP1-DT in KIRC. RT-qPCR, Kaplan-Meier survival analysis, Cox regression analysis, and nomogram analysis were utilized to determine the expression and effects of CTBP1-DT on survival. The subcellular localization of CTBP1-DT was determined using RNA fluorescence in situ hybridization (FISH). To investigate the functions of CTBP1-DT in regulating KIRC cell proliferation, migration, invasion, lipid synthesis, and apoptosis, we conducted CCK8, EdU, Transwell, and Oil Red O staining and cell apoptosis staining assays. The relationships between CTBP1-DT and the tumor microenvironment were investigated with multiple bioinformatics analysis algorithms and databases, including CYBERSORT, TIMER2, Spearman correlation test, tumor mutation burden (TMB), microsatellite instability (MSI), and immunophenoscore (IPS). According to our results, CTBP1-DT is a lncRNA located in the nucleus that is significantly upregulated in KIRC and is correlated with better clinical outcomes. Downregulating CTBP1-DT inhibited cell viability, migration, invasion, and lipid synthesis but triggered cell apoptosis. Additionally, we explored the potential effect of CTBP1-DT in regulating immune cell infiltration in KIRC and other malignancies. Furthermore, CTBP1-DT could be used to predict the effectiveness of targeted drugs and immune checkpoint inhibitors. In conclusion, we identified CTBP1-DT as a potential immunological biomarker and discovered the potential role of CTBP1-DT in regulating lipid synthesis and apoptosis resistance.</description><subject>Alcohol Oxidoreductases - genetics</subject><subject>Alcohol Oxidoreductases - metabolism</subject><subject>Apoptosis</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Carcinoma, Renal Cell - genetics</subject><subject>Carcinoma, Renal Cell - immunology</subject><subject>Carcinoma, Renal Cell - metabolism</subject><subject>Carcinoma, Renal Cell - pathology</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>CTBP1-DT</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Kidney Neoplasms - genetics</subject><subject>Kidney Neoplasms - immunology</subject><subject>Kidney Neoplasms - metabolism</subject><subject>Kidney Neoplasms - pathology</subject><subject>KIRC</subject><subject>Lipid</subject><subject>Lipids</subject><subject>lncRNA</subject><subject>Male</subject><subject>Prognosis</subject><subject>RNA, Long Noncoding - genetics</subject><subject>Tumor Microenvironment</subject><issn>0378-1119</issn><issn>1879-0038</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1PGzEQhi1EBSnlD_RQ-chlU3_t2pF6gdCPiEigKpwtr3cCTnftxXYq5d_Xq0CPzGU0o_d9NfMg9JmSOSW0-bqbP4GHOSNMzKlQgvATNKNKLipCuDpFM8Klqiili3P0MaUdKVXX7Aydc1Wzsmcz5Fcd-Oy2B7zc3DzQ6naDTcLGYzcMex_68OSs6XHrwmDiH4g4P5uMxxiGkCHh3o2uw-ng8zMkNxk7bMYw5jBNcdpl4y1g5_Hd6vfyE_qwNX2Cy9d-gR5_fN8sf1Xr-5-r5fW6srxuciUoZ4oKI4FwQWUjjJW1kkApF6ztOAhiCesaohhXlBFh65bJhte25dIKwy_Q1TG3XPqyh5T14JKFvjcewj5ptpCCEMn4okjZUWpjSCnCVo_RlWcPmhI9cdY7PXHWE2d95FxMX17z9-0A3X_LG9gi-HYUQPnyr4Ook3VQSHQugs26C-69_H-g9I0J</recordid><startdate>20240701</startdate><enddate>20240701</enddate><creator>Li, Haolin</creator><creator>Fei, Mintian</creator><creator>Zhang, Yi</creator><creator>Xu, Qili</creator><creator>Feng, Rui</creator><creator>Cao, Jing</creator><creator>Qu, Yan</creator><creator>Xiao, Haibing</creator><general>Elsevier B.V</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>7X8</scope><orcidid>https://orcid.org/0000-0001-8181-0125</orcidid></search><sort><creationdate>20240701</creationdate><title>Identify CTBP1-DT as an immunological biomarker that promotes lipid synthesis and apoptosis resistance in KIRC</title><author>Li, Haolin ; Fei, Mintian ; Zhang, Yi ; Xu, Qili ; Feng, Rui ; Cao, Jing ; Qu, Yan ; Xiao, Haibing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c356t-4132814a7e0341764ac7587e11342bd3e40c02d6082381204c5b27635cb37c4a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Alcohol Oxidoreductases - genetics</topic><topic>Alcohol Oxidoreductases - metabolism</topic><topic>Apoptosis</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Carcinoma, Renal Cell - genetics</topic><topic>Carcinoma, Renal Cell - immunology</topic><topic>Carcinoma, Renal Cell - metabolism</topic><topic>Carcinoma, Renal Cell - pathology</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>CTBP1-DT</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Kidney Neoplasms - genetics</topic><topic>Kidney Neoplasms - immunology</topic><topic>Kidney Neoplasms - metabolism</topic><topic>Kidney Neoplasms - pathology</topic><topic>KIRC</topic><topic>Lipid</topic><topic>Lipids</topic><topic>lncRNA</topic><topic>Male</topic><topic>Prognosis</topic><topic>RNA, Long Noncoding - genetics</topic><topic>Tumor Microenvironment</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Haolin</creatorcontrib><creatorcontrib>Fei, Mintian</creatorcontrib><creatorcontrib>Zhang, Yi</creatorcontrib><creatorcontrib>Xu, Qili</creatorcontrib><creatorcontrib>Feng, Rui</creatorcontrib><creatorcontrib>Cao, Jing</creatorcontrib><creatorcontrib>Qu, Yan</creatorcontrib><creatorcontrib>Xiao, Haibing</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>Gene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Haolin</au><au>Fei, Mintian</au><au>Zhang, Yi</au><au>Xu, Qili</au><au>Feng, Rui</au><au>Cao, Jing</au><au>Qu, Yan</au><au>Xiao, Haibing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Identify CTBP1-DT as an immunological biomarker that promotes lipid synthesis and apoptosis resistance in KIRC</atitle><jtitle>Gene</jtitle><addtitle>Gene</addtitle><date>2024-07-01</date><risdate>2024</risdate><volume>914</volume><spage>148403</spage><epage>148403</epage><pages>148403-148403</pages><artnum>148403</artnum><issn>0378-1119</issn><eissn>1879-0038</eissn><abstract>•CTBP1-DT is a lncRNA located in the nucleus that is significantly upregulated in clear cell renal cell carcinoma.•Downregulate CTBP1-DT could inhibit cell lipid content.•CTBP1-DT is linked with immune cell infiltration in clear cell renal cell carcinoma, especially macrophages. Recently, mounting evidence has highlighted the essential function of the C-terminal binding protein-1 divergent transcript (CTBP1-DT) in malignancies. However, its role in kidney renal clear cell carcinoma (KIRC) remains largely unknown. Our study aimed to identify the potential function of CTBP1-DT in KIRC. RT-qPCR, Kaplan-Meier survival analysis, Cox regression analysis, and nomogram analysis were utilized to determine the expression and effects of CTBP1-DT on survival. The subcellular localization of CTBP1-DT was determined using RNA fluorescence in situ hybridization (FISH). To investigate the functions of CTBP1-DT in regulating KIRC cell proliferation, migration, invasion, lipid synthesis, and apoptosis, we conducted CCK8, EdU, Transwell, and Oil Red O staining and cell apoptosis staining assays. The relationships between CTBP1-DT and the tumor microenvironment were investigated with multiple bioinformatics analysis algorithms and databases, including CYBERSORT, TIMER2, Spearman correlation test, tumor mutation burden (TMB), microsatellite instability (MSI), and immunophenoscore (IPS). According to our results, CTBP1-DT is a lncRNA located in the nucleus that is significantly upregulated in KIRC and is correlated with better clinical outcomes. Downregulating CTBP1-DT inhibited cell viability, migration, invasion, and lipid synthesis but triggered cell apoptosis. Additionally, we explored the potential effect of CTBP1-DT in regulating immune cell infiltration in KIRC and other malignancies. Furthermore, CTBP1-DT could be used to predict the effectiveness of targeted drugs and immune checkpoint inhibitors. In conclusion, we identified CTBP1-DT as a potential immunological biomarker and discovered the potential role of CTBP1-DT in regulating lipid synthesis and apoptosis resistance.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>38521112</pmid><doi>10.1016/j.gene.2024.148403</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0001-8181-0125</orcidid></addata></record>
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subjects Alcohol Oxidoreductases - genetics
Alcohol Oxidoreductases - metabolism
Apoptosis
Biomarkers, Tumor - genetics
Biomarkers, Tumor - metabolism
Carcinoma, Renal Cell - genetics
Carcinoma, Renal Cell - immunology
Carcinoma, Renal Cell - metabolism
Carcinoma, Renal Cell - pathology
Cell Line, Tumor
Cell Movement
Cell Proliferation
CTBP1-DT
DNA-Binding Proteins - genetics
DNA-Binding Proteins - metabolism
Female
Gene Expression Regulation, Neoplastic
Humans
Kidney Neoplasms - genetics
Kidney Neoplasms - immunology
Kidney Neoplasms - metabolism
Kidney Neoplasms - pathology
KIRC
Lipid
Lipids
lncRNA
Male
Prognosis
RNA, Long Noncoding - genetics
Tumor Microenvironment
title Identify CTBP1-DT as an immunological biomarker that promotes lipid synthesis and apoptosis resistance in KIRC
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