Nuclear protein NOP2 serves as a poor-prognosis predictor of LUAD and aggravates the malignancy of lung adenocarcinoma cells
Recent studies have shown that NOP2, a nucleolar protein, is up-regulated in various cancers, suggesting a potential link to tumor aggressiveness and unfavorable outcomes. This study examines NOP2's role in lung adenocarcinoma (LUAD), a context where its implications remain unclear. Utilizing b...
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| description | Recent studies have shown that NOP2, a nucleolar protein, is up-regulated in various cancers, suggesting a potential link to tumor aggressiveness and unfavorable outcomes. This study examines NOP2's role in lung adenocarcinoma (LUAD), a context where its implications remain unclear. Utilizing bioinformatics, we assessed 513 LUAD and 59 normal tissue samples from The Cancer Genome Atlas (TCGA) to explore NOP2's diagnostic and prognostic significance in LUAD. Additionally, in vitro experiments compared NOP2 expression between Beas-2b and A549 cells. Advanced databases and analytical tools, including LINKEDOMICS, STRING, and TISIDB, were employed to further elucidate NOP2's association with LUAD. Our findings indicate a significantly higher expression of NOP2 mRNA and protein in A549 cells compared to Beas-2b cells (
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| doi_str_mv | 10.1007/s10142-024-01337-8 |
| format | Article |
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P
< 0.001). In LUAD, elevated NOP2 levels were linked to decreased Overall Survival (OS) and advanced clinical stages. Univariate Cox analysis revealed that high NOP2 expression correlated with poorer OS in LUAD (
P
< 0.01), a finding independently supported by multivariate Cox analysis (
P
< 0.05). The relationship between NOP2 expression and LUAD risk was presented via a Nomogram. Additionally, Gene Set Enrichment Analysis (GSEA) identified seven NOP2-related signaling pathways. A focal point of our research was the interplay between NOP2 and tumor-immune interactions. Notably, a negative correlation was observed between NOP2 expression and the immune infiltration levels of macrophages, neutrophils, mast cells, Natural Killer (NK) cells, and CD8 + T cells in LUAD. Moreover, the expression of NOP2 was related to the sensitivity of various chemotherapeutic drugs. In vitro, we found that downregulating NOP2 can decrease the proliferation, migration and invasion of A549 cells. Furthermore, NOP2 can regulate Caspase3-mediated apoptosis. Collectively, particularly regarding prognosis, immune infiltration and vitro experiments, these findings suggest NOP2's potential of serving as a poor-prognostic biomarker for LUAD and aggravating the malignancy of lung adenocarcinoma cells.</description><identifier>ISSN: 1438-793X</identifier><identifier>EISSN: 1438-7948</identifier><identifier>DOI: 10.1007/s10142-024-01337-8</identifier><identifier>PMID: 38489049</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Adenocarcinoma ; Animal Genetics and Genomics ; Antineoplastic drugs ; Apoptosis ; Biochemistry ; Bioinformatics ; Biomarkers ; Biomedical and Life Sciences ; Cancer ; CD8 antigen ; Cell Biology ; Cell growth ; Cell proliferation ; Chemotherapy ; Drug resistance ; Gene expression ; Gene set enrichment analysis ; Genomes ; Immunosuppressive agents ; Infiltration ; Leukocyte migration ; Leukocytes (neutrophilic) ; Life Sciences ; Lung cancer ; Lymphocytes T ; Macrophages ; Malignancy ; Mast cells ; Medical prognosis ; Metastases ; Microbial Genetics and Genomics ; mRNA ; Natural killer cells ; Nucleoli ; Original Article ; Plant Genetics and Genomics ; Prognosis ; Proteins ; Survival analysis ; Tumors</subject><ispartof>Functional & integrative genomics, 2024-04, Vol.24 (2), p.58-58, Article 58</ispartof><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c326t-e9a16497e38b22207f80d6dbd6a5e610f4a66c0d8d2f743fb55c66972555858a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10142-024-01337-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10142-024-01337-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38489049$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Qin, Weizhuo</creatorcontrib><creatorcontrib>Fei, Gaoqiang</creatorcontrib><creatorcontrib>Zhou, Qian</creatorcontrib><creatorcontrib>Li, Zhijie</creatorcontrib><creatorcontrib>Li, Wei</creatorcontrib><creatorcontrib>Wei, Pingmin</creatorcontrib><title>Nuclear protein NOP2 serves as a poor-prognosis predictor of LUAD and aggravates the malignancy of lung adenocarcinoma cells</title><title>Functional & integrative genomics</title><addtitle>Funct Integr Genomics</addtitle><addtitle>Funct Integr Genomics</addtitle><description>Recent studies have shown that NOP2, a nucleolar protein, is up-regulated in various cancers, suggesting a potential link to tumor aggressiveness and unfavorable outcomes. This study examines NOP2's role in lung adenocarcinoma (LUAD), a context where its implications remain unclear. Utilizing bioinformatics, we assessed 513 LUAD and 59 normal tissue samples from The Cancer Genome Atlas (TCGA) to explore NOP2's diagnostic and prognostic significance in LUAD. Additionally, in vitro experiments compared NOP2 expression between Beas-2b and A549 cells. Advanced databases and analytical tools, including LINKEDOMICS, STRING, and TISIDB, were employed to further elucidate NOP2's association with LUAD. Our findings indicate a significantly higher expression of NOP2 mRNA and protein in A549 cells compared to Beas-2b cells (
P
< 0.001). In LUAD, elevated NOP2 levels were linked to decreased Overall Survival (OS) and advanced clinical stages. Univariate Cox analysis revealed that high NOP2 expression correlated with poorer OS in LUAD (
P
< 0.01), a finding independently supported by multivariate Cox analysis (
P
< 0.05). The relationship between NOP2 expression and LUAD risk was presented via a Nomogram. Additionally, Gene Set Enrichment Analysis (GSEA) identified seven NOP2-related signaling pathways. A focal point of our research was the interplay between NOP2 and tumor-immune interactions. Notably, a negative correlation was observed between NOP2 expression and the immune infiltration levels of macrophages, neutrophils, mast cells, Natural Killer (NK) cells, and CD8 + T cells in LUAD. Moreover, the expression of NOP2 was related to the sensitivity of various chemotherapeutic drugs. In vitro, we found that downregulating NOP2 can decrease the proliferation, migration and invasion of A549 cells. Furthermore, NOP2 can regulate Caspase3-mediated apoptosis. Collectively, particularly regarding prognosis, immune infiltration and vitro experiments, these findings suggest NOP2's potential of serving as a poor-prognostic biomarker for LUAD and aggravating the malignancy of lung adenocarcinoma cells.</description><subject>Adenocarcinoma</subject><subject>Animal Genetics and Genomics</subject><subject>Antineoplastic drugs</subject><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Bioinformatics</subject><subject>Biomarkers</subject><subject>Biomedical and Life Sciences</subject><subject>Cancer</subject><subject>CD8 antigen</subject><subject>Cell Biology</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>Chemotherapy</subject><subject>Drug resistance</subject><subject>Gene expression</subject><subject>Gene set enrichment analysis</subject><subject>Genomes</subject><subject>Immunosuppressive agents</subject><subject>Infiltration</subject><subject>Leukocyte migration</subject><subject>Leukocytes (neutrophilic)</subject><subject>Life Sciences</subject><subject>Lung cancer</subject><subject>Lymphocytes T</subject><subject>Macrophages</subject><subject>Malignancy</subject><subject>Mast cells</subject><subject>Medical prognosis</subject><subject>Metastases</subject><subject>Microbial Genetics and Genomics</subject><subject>mRNA</subject><subject>Natural killer cells</subject><subject>Nucleoli</subject><subject>Original Article</subject><subject>Plant Genetics and Genomics</subject><subject>Prognosis</subject><subject>Proteins</subject><subject>Survival analysis</subject><subject>Tumors</subject><issn>1438-793X</issn><issn>1438-7948</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNp9kU1LHTEUhkOx1K_-ARcScNPNtPmeZCna2sJFu6jgLpybZMaRmeSazAhCf3xze62FLgqBBM7zvuecvAidUPKREtJ-KpRQwRrCREMo522j36ADKrhuWiP03uub3-2jw1IeCCGSGP4O7XMttCHCHKCf14sbA2S8yWkOQ8TXN98ZLiE_hYKhHrxJKTe12sdUhlK54Ac3p4xTh1e355cYosfQ9xmeYK6i-T7gCcahjxDd85Yal9hj8CEmB9kNMU2AXRjHcozedjCW8P7lPkK3Xz7_uPjarG6uvl2crxrHmZqbYIAqYdrA9ZoxRtpOE6_82iuQQVHSCVDKEa8961rBu7WUTinTMimllhr4Efqw861rPC6hzHYaynYCiCEtxTIjNTMVNRU9-wd9SEuOdbot1SpR_1lViu0ol1MpOXR2k4cJ8rOlxG6zsbtsbM3G_s7G6io6fbFe1lPwr5I_YVSA74BSS7EP-W_v_9j-AqwQma8</recordid><startdate>20240401</startdate><enddate>20240401</enddate><creator>Qin, Weizhuo</creator><creator>Fei, Gaoqiang</creator><creator>Zhou, Qian</creator><creator>Li, Zhijie</creator><creator>Li, Wei</creator><creator>Wei, Pingmin</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20240401</creationdate><title>Nuclear protein NOP2 serves as a poor-prognosis predictor of LUAD and aggravates the malignancy of lung adenocarcinoma cells</title><author>Qin, Weizhuo ; Fei, Gaoqiang ; Zhou, Qian ; Li, Zhijie ; Li, Wei ; Wei, Pingmin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c326t-e9a16497e38b22207f80d6dbd6a5e610f4a66c0d8d2f743fb55c66972555858a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Adenocarcinoma</topic><topic>Animal Genetics and Genomics</topic><topic>Antineoplastic drugs</topic><topic>Apoptosis</topic><topic>Biochemistry</topic><topic>Bioinformatics</topic><topic>Biomarkers</topic><topic>Biomedical and Life Sciences</topic><topic>Cancer</topic><topic>CD8 antigen</topic><topic>Cell Biology</topic><topic>Cell growth</topic><topic>Cell proliferation</topic><topic>Chemotherapy</topic><topic>Drug resistance</topic><topic>Gene expression</topic><topic>Gene set enrichment analysis</topic><topic>Genomes</topic><topic>Immunosuppressive agents</topic><topic>Infiltration</topic><topic>Leukocyte migration</topic><topic>Leukocytes (neutrophilic)</topic><topic>Life Sciences</topic><topic>Lung cancer</topic><topic>Lymphocytes T</topic><topic>Macrophages</topic><topic>Malignancy</topic><topic>Mast cells</topic><topic>Medical prognosis</topic><topic>Metastases</topic><topic>Microbial Genetics and Genomics</topic><topic>mRNA</topic><topic>Natural killer cells</topic><topic>Nucleoli</topic><topic>Original Article</topic><topic>Plant Genetics and Genomics</topic><topic>Prognosis</topic><topic>Proteins</topic><topic>Survival analysis</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Qin, Weizhuo</creatorcontrib><creatorcontrib>Fei, Gaoqiang</creatorcontrib><creatorcontrib>Zhou, Qian</creatorcontrib><creatorcontrib>Li, Zhijie</creatorcontrib><creatorcontrib>Li, Wei</creatorcontrib><creatorcontrib>Wei, Pingmin</creatorcontrib><collection>PubMed</collection><collection>CrossRef</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>Functional & integrative genomics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Qin, Weizhuo</au><au>Fei, Gaoqiang</au><au>Zhou, Qian</au><au>Li, Zhijie</au><au>Li, Wei</au><au>Wei, Pingmin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nuclear protein NOP2 serves as a poor-prognosis predictor of LUAD and aggravates the malignancy of lung adenocarcinoma cells</atitle><jtitle>Functional & integrative genomics</jtitle><stitle>Funct Integr Genomics</stitle><addtitle>Funct Integr Genomics</addtitle><date>2024-04-01</date><risdate>2024</risdate><volume>24</volume><issue>2</issue><spage>58</spage><epage>58</epage><pages>58-58</pages><artnum>58</artnum><issn>1438-793X</issn><eissn>1438-7948</eissn><abstract>Recent studies have shown that NOP2, a nucleolar protein, is up-regulated in various cancers, suggesting a potential link to tumor aggressiveness and unfavorable outcomes. This study examines NOP2's role in lung adenocarcinoma (LUAD), a context where its implications remain unclear. Utilizing bioinformatics, we assessed 513 LUAD and 59 normal tissue samples from The Cancer Genome Atlas (TCGA) to explore NOP2's diagnostic and prognostic significance in LUAD. Additionally, in vitro experiments compared NOP2 expression between Beas-2b and A549 cells. Advanced databases and analytical tools, including LINKEDOMICS, STRING, and TISIDB, were employed to further elucidate NOP2's association with LUAD. Our findings indicate a significantly higher expression of NOP2 mRNA and protein in A549 cells compared to Beas-2b cells (
P
< 0.001). In LUAD, elevated NOP2 levels were linked to decreased Overall Survival (OS) and advanced clinical stages. Univariate Cox analysis revealed that high NOP2 expression correlated with poorer OS in LUAD (
P
< 0.01), a finding independently supported by multivariate Cox analysis (
P
< 0.05). The relationship between NOP2 expression and LUAD risk was presented via a Nomogram. Additionally, Gene Set Enrichment Analysis (GSEA) identified seven NOP2-related signaling pathways. A focal point of our research was the interplay between NOP2 and tumor-immune interactions. Notably, a negative correlation was observed between NOP2 expression and the immune infiltration levels of macrophages, neutrophils, mast cells, Natural Killer (NK) cells, and CD8 + T cells in LUAD. Moreover, the expression of NOP2 was related to the sensitivity of various chemotherapeutic drugs. In vitro, we found that downregulating NOP2 can decrease the proliferation, migration and invasion of A549 cells. Furthermore, NOP2 can regulate Caspase3-mediated apoptosis. Collectively, particularly regarding prognosis, immune infiltration and vitro experiments, these findings suggest NOP2's potential of serving as a poor-prognostic biomarker for LUAD and aggravating the malignancy of lung adenocarcinoma cells.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>38489049</pmid><doi>10.1007/s10142-024-01337-8</doi><tpages>1</tpages></addata></record> |
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| subjects | Adenocarcinoma Animal Genetics and Genomics Antineoplastic drugs Apoptosis Biochemistry Bioinformatics Biomarkers Biomedical and Life Sciences Cancer CD8 antigen Cell Biology Cell growth Cell proliferation Chemotherapy Drug resistance Gene expression Gene set enrichment analysis Genomes Immunosuppressive agents Infiltration Leukocyte migration Leukocytes (neutrophilic) Life Sciences Lung cancer Lymphocytes T Macrophages Malignancy Mast cells Medical prognosis Metastases Microbial Genetics and Genomics mRNA Natural killer cells Nucleoli Original Article Plant Genetics and Genomics Prognosis Proteins Survival analysis Tumors |
| title | Nuclear protein NOP2 serves as a poor-prognosis predictor of LUAD and aggravates the malignancy of lung adenocarcinoma cells |
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