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NEIL3 may act as a potential prognostic biomarker for lung adenocarcinoma

Lung adenocarcinoma (LUAD) is the leading cause of cancer-related death. This study aimed to develop and validate reliable prognostic biomarkers and signature. Differentially expressed genes were identified based on three Gene Expression Omnibus (GEO) datasets. Based on 1052 samples' data from...

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Published in:Cancer cell international 2021-04, Vol.21 (1), p.228-228, Article 228
Main Authors: Zhao, Cui, Liu, Jian, Zhou, Haomiao, Qian, Xin, Sun, Hui, Chen, Xuewen, Zheng, Miaosen, Bian, Tingting, Liu, Lei, Liu, Yifei, Zhang, Jianguo
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creator Zhao, Cui
Liu, Jian
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Sun, Hui
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Zheng, Miaosen
Bian, Tingting
Liu, Lei
Liu, Yifei
Zhang, Jianguo
description Lung adenocarcinoma (LUAD) is the leading cause of cancer-related death. This study aimed to develop and validate reliable prognostic biomarkers and signature. Differentially expressed genes were identified based on three Gene Expression Omnibus (GEO) datasets. Based on 1052 samples' data from our cohort, GEO and The Cancer Genome Atlas, we explored the relationship of clinicopathological features and NEIL3 expression to determine clinical effect of NEIL3 in LUAD. Western blotting (22 pairs of tumor and normal tissues), Real-time quantitative PCR (19 pairs of tumor and normal tissues), and immunohistochemical analyses (406-tumor tissues subjected to microarray) were conducted. TIMER and ImmuCellAI analyzed relationship between NEIL3 expression and the abundance of tumor-infiltrating immune cells in LUAD. The co-expressed-gene prognostic signature was established based on the Cox regression analysis. This study identified 502 common differentially expressed genes and confirmed that NEIL3 was significantly overexpressed in LUAD samples (P 
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This study aimed to develop and validate reliable prognostic biomarkers and signature. Differentially expressed genes were identified based on three Gene Expression Omnibus (GEO) datasets. Based on 1052 samples' data from our cohort, GEO and The Cancer Genome Atlas, we explored the relationship of clinicopathological features and NEIL3 expression to determine clinical effect of NEIL3 in LUAD. Western blotting (22 pairs of tumor and normal tissues), Real-time quantitative PCR (19 pairs of tumor and normal tissues), and immunohistochemical analyses (406-tumor tissues subjected to microarray) were conducted. TIMER and ImmuCellAI analyzed relationship between NEIL3 expression and the abundance of tumor-infiltrating immune cells in LUAD. The co-expressed-gene prognostic signature was established based on the Cox regression analysis. This study identified 502 common differentially expressed genes and confirmed that NEIL3 was significantly overexpressed in LUAD samples (P &lt; 0.001). Increased NEIL3 expression was related to advanced stage, larger tumor size and poor overall survival (p &lt; 0.001) in three LUAD cohorts. The proportions of natural T regulatory cells and induced T regulatory cells increased in the high NEIL3 group, whereas those of B cells, Th17 cells and dendritic cells decreased. Gene set enrichment analysis indicated that NEIL3 may activate cell cycle progression and P53 signaling pathway, leading to poor outcomes. We identified nine prognosis-associated hub genes among 370 genes co-expressed with NEIL3. A 10-gene prognostic signature including NEIL3 and nine key co-expressed genes was constructed. Higher risk-score was correlated with more advanced stage, larger tumor size and worse outcome (p &lt; 0.05). Finally, the signature was verified in test cohort (GSE50081) with superior diagnostic accuracy. This study suggested that NEIL3 has the potential to be an immune-related therapeutic target and an independent predictor of LUAD prognosis. We also developed a prognostic signature for LUAD with a precise diagnostic accuracy.</description><identifier>ISSN: 1475-2867</identifier><identifier>EISSN: 1475-2867</identifier><identifier>DOI: 10.1186/s12935-021-01938-4</identifier><identifier>PMID: 33879165</identifier><language>eng</language><publisher>England: BioMed Central</publisher><subject>Adenocarcinoma ; Bioinformatics ; Biomarkers ; Cell cycle ; Dendritic cells ; DNA microarrays ; Gene expression ; Gene set enrichment analysis ; Genomes ; Helper cells ; Immunohistochemistry ; Immunoregulation ; Lung adenocarcinoma ; Lung cancer ; Lymphatic system ; Lymphocytes B ; Lymphocytes T ; Medical prognosis ; Medical research ; Metastasis ; NEIL3 ; p53 Protein ; Pathology ; Polymerase chain reaction ; Primary Research ; Prognosis ; Prognostic signature ; Proteins ; Real-time quantitative PCR ; Regression analysis ; Signal transduction ; Software ; Therapeutic targets ; Tumor-infiltrating lymphocytes ; Values ; Western blotting</subject><ispartof>Cancer cell international, 2021-04, Vol.21 (1), p.228-228, Article 228</ispartof><rights>2021. 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This study aimed to develop and validate reliable prognostic biomarkers and signature. Differentially expressed genes were identified based on three Gene Expression Omnibus (GEO) datasets. Based on 1052 samples' data from our cohort, GEO and The Cancer Genome Atlas, we explored the relationship of clinicopathological features and NEIL3 expression to determine clinical effect of NEIL3 in LUAD. Western blotting (22 pairs of tumor and normal tissues), Real-time quantitative PCR (19 pairs of tumor and normal tissues), and immunohistochemical analyses (406-tumor tissues subjected to microarray) were conducted. TIMER and ImmuCellAI analyzed relationship between NEIL3 expression and the abundance of tumor-infiltrating immune cells in LUAD. The co-expressed-gene prognostic signature was established based on the Cox regression analysis. This study identified 502 common differentially expressed genes and confirmed that NEIL3 was significantly overexpressed in LUAD samples (P &lt; 0.001). Increased NEIL3 expression was related to advanced stage, larger tumor size and poor overall survival (p &lt; 0.001) in three LUAD cohorts. The proportions of natural T regulatory cells and induced T regulatory cells increased in the high NEIL3 group, whereas those of B cells, Th17 cells and dendritic cells decreased. Gene set enrichment analysis indicated that NEIL3 may activate cell cycle progression and P53 signaling pathway, leading to poor outcomes. We identified nine prognosis-associated hub genes among 370 genes co-expressed with NEIL3. A 10-gene prognostic signature including NEIL3 and nine key co-expressed genes was constructed. Higher risk-score was correlated with more advanced stage, larger tumor size and worse outcome (p &lt; 0.05). Finally, the signature was verified in test cohort (GSE50081) with superior diagnostic accuracy. This study suggested that NEIL3 has the potential to be an immune-related therapeutic target and an independent predictor of LUAD prognosis. 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This study aimed to develop and validate reliable prognostic biomarkers and signature. Differentially expressed genes were identified based on three Gene Expression Omnibus (GEO) datasets. Based on 1052 samples' data from our cohort, GEO and The Cancer Genome Atlas, we explored the relationship of clinicopathological features and NEIL3 expression to determine clinical effect of NEIL3 in LUAD. Western blotting (22 pairs of tumor and normal tissues), Real-time quantitative PCR (19 pairs of tumor and normal tissues), and immunohistochemical analyses (406-tumor tissues subjected to microarray) were conducted. TIMER and ImmuCellAI analyzed relationship between NEIL3 expression and the abundance of tumor-infiltrating immune cells in LUAD. The co-expressed-gene prognostic signature was established based on the Cox regression analysis. This study identified 502 common differentially expressed genes and confirmed that NEIL3 was significantly overexpressed in LUAD samples (P &lt; 0.001). Increased NEIL3 expression was related to advanced stage, larger tumor size and poor overall survival (p &lt; 0.001) in three LUAD cohorts. The proportions of natural T regulatory cells and induced T regulatory cells increased in the high NEIL3 group, whereas those of B cells, Th17 cells and dendritic cells decreased. Gene set enrichment analysis indicated that NEIL3 may activate cell cycle progression and P53 signaling pathway, leading to poor outcomes. We identified nine prognosis-associated hub genes among 370 genes co-expressed with NEIL3. A 10-gene prognostic signature including NEIL3 and nine key co-expressed genes was constructed. Higher risk-score was correlated with more advanced stage, larger tumor size and worse outcome (p &lt; 0.05). Finally, the signature was verified in test cohort (GSE50081) with superior diagnostic accuracy. This study suggested that NEIL3 has the potential to be an immune-related therapeutic target and an independent predictor of LUAD prognosis. We also developed a prognostic signature for LUAD with a precise diagnostic accuracy.</abstract><cop>England</cop><pub>BioMed Central</pub><pmid>33879165</pmid><doi>10.1186/s12935-021-01938-4</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0003-2315-4822</orcidid><oa>free_for_read</oa></addata></record>
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subjects Adenocarcinoma
Bioinformatics
Biomarkers
Cell cycle
Dendritic cells
DNA microarrays
Gene expression
Gene set enrichment analysis
Genomes
Helper cells
Immunohistochemistry
Immunoregulation
Lung adenocarcinoma
Lung cancer
Lymphatic system
Lymphocytes B
Lymphocytes T
Medical prognosis
Medical research
Metastasis
NEIL3
p53 Protein
Pathology
Polymerase chain reaction
Primary Research
Prognosis
Prognostic signature
Proteins
Real-time quantitative PCR
Regression analysis
Signal transduction
Software
Therapeutic targets
Tumor-infiltrating lymphocytes
Values
Western blotting
title NEIL3 may act as a potential prognostic biomarker for lung adenocarcinoma
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