A pan-cancer analysis of the oncogenic role of N-acetyltransferase 8 like in human cancer

Abstract Background N-Acetyltransferase 8 Like (NAT8L) inhibits natural killer (NK)/T-cell cytotoxicity by impairing the formation of the immunological synapse via N-acetylaspartate (NAA). Existing research has predominantly focused on the metabolic functions of NAT8L, particularly in adipose tissue...

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Main Authors: Jiamin Chen, Fanglin Shao, Shuxia Zhang, Youliang Qian, Mei Chen
Format: Article
Language:English
Published: Springer 2024-12-01
Series:Discover Oncology
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Online Access:https://doi.org/10.1007/s12672-024-01605-w
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author Jiamin Chen
Fanglin Shao
Shuxia Zhang
Youliang Qian
Mei Chen
author_facet Jiamin Chen
Fanglin Shao
Shuxia Zhang
Youliang Qian
Mei Chen
author_sort Jiamin Chen
collection DOAJ
description Abstract Background N-Acetyltransferase 8 Like (NAT8L) inhibits natural killer (NK)/T-cell cytotoxicity by impairing the formation of the immunological synapse via N-acetylaspartate (NAA). Existing research has predominantly focused on the metabolic functions of NAT8L, particularly in adipose tissues and myelination in the brain. However, in contrast to other N-acetyltransferases such as NAT1 and NAT2, the role of NAT8L in cancer has been less extensively studied. In this study, we conducted a comprehensive pan-cancer analysis to investigate the carcinogenic role of NAT8L in human cancers. Methods We utilized the standardized TCGA pan-cancer dataset to analyze differential expression, clinical prognosis, gene mutation, immune infiltration, epigenetic modification, tumor stemness, and heterogeneity. Additionally, we evaluated the sensitivity of NAT8L to small molecule drugs using the GDSC and CTRP databases. Results In this study, we identified that NAT8L expression was upregulated in 6 cancers and downregulated in 12 compared to normal tissues. We analyzed its prognostic value in 5 tumor types (KIRP, COAD, COADREAD, GBMLGG, LUSC) and found correlations with overall survival (OS), disease-specific survival (DSS), and progression-free interval (PFI). Furthermore, NAT8L expression was significantly correlated with levels of most immune checkpoints, immunomodulators, and immune cell infiltration. The mutation frequencies for bladder cancer (BLCA), glioblastoma multiforme and glioma (GBMLGG), lower-grade glioma (LGG), and KIRP were 1.2%, 0.9%, 0.8%, and 0.4%, respectively. Conclusion Our findings suggest that NAT8L may serve as a potential prognostic marker and therapeutic target across a variety of cancers, particularly in KIRP, COAD, COADREAD, GBMLGG, and lung squamous cell carcinoma (LUSC).
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spelling doaj-art-a4872df5b040453da9bb337894bd17c82024-12-22T12:35:11ZengSpringerDiscover Oncology2730-60112024-12-0115111710.1007/s12672-024-01605-wA pan-cancer analysis of the oncogenic role of N-acetyltransferase 8 like in human cancerJiamin Chen0Fanglin Shao1Shuxia Zhang2Youliang Qian3Mei Chen4Institute of Clinical Pathology& Department of Pathology, Shantou University Medical CollegeChengdu Basebio CompanyResearch Core Facilities, West China Hospital, Sichuan UniversityDepartment of Urology, Chengdu Second People’s HospitalDepartment of Urology, Yaan People’s HospitalAbstract Background N-Acetyltransferase 8 Like (NAT8L) inhibits natural killer (NK)/T-cell cytotoxicity by impairing the formation of the immunological synapse via N-acetylaspartate (NAA). Existing research has predominantly focused on the metabolic functions of NAT8L, particularly in adipose tissues and myelination in the brain. However, in contrast to other N-acetyltransferases such as NAT1 and NAT2, the role of NAT8L in cancer has been less extensively studied. In this study, we conducted a comprehensive pan-cancer analysis to investigate the carcinogenic role of NAT8L in human cancers. Methods We utilized the standardized TCGA pan-cancer dataset to analyze differential expression, clinical prognosis, gene mutation, immune infiltration, epigenetic modification, tumor stemness, and heterogeneity. Additionally, we evaluated the sensitivity of NAT8L to small molecule drugs using the GDSC and CTRP databases. Results In this study, we identified that NAT8L expression was upregulated in 6 cancers and downregulated in 12 compared to normal tissues. We analyzed its prognostic value in 5 tumor types (KIRP, COAD, COADREAD, GBMLGG, LUSC) and found correlations with overall survival (OS), disease-specific survival (DSS), and progression-free interval (PFI). Furthermore, NAT8L expression was significantly correlated with levels of most immune checkpoints, immunomodulators, and immune cell infiltration. The mutation frequencies for bladder cancer (BLCA), glioblastoma multiforme and glioma (GBMLGG), lower-grade glioma (LGG), and KIRP were 1.2%, 0.9%, 0.8%, and 0.4%, respectively. Conclusion Our findings suggest that NAT8L may serve as a potential prognostic marker and therapeutic target across a variety of cancers, particularly in KIRP, COAD, COADREAD, GBMLGG, and lung squamous cell carcinoma (LUSC).https://doi.org/10.1007/s12672-024-01605-wPan-cancerTumor immune microenvironmentPrognosisN-Acetyltransferase 8 like
spellingShingle Jiamin Chen
Fanglin Shao
Shuxia Zhang
Youliang Qian
Mei Chen
A pan-cancer analysis of the oncogenic role of N-acetyltransferase 8 like in human cancer
Discover Oncology
Pan-cancer
Tumor immune microenvironment
Prognosis
N-Acetyltransferase 8 like
title A pan-cancer analysis of the oncogenic role of N-acetyltransferase 8 like in human cancer
title_full A pan-cancer analysis of the oncogenic role of N-acetyltransferase 8 like in human cancer
title_fullStr A pan-cancer analysis of the oncogenic role of N-acetyltransferase 8 like in human cancer
title_full_unstemmed A pan-cancer analysis of the oncogenic role of N-acetyltransferase 8 like in human cancer
title_short A pan-cancer analysis of the oncogenic role of N-acetyltransferase 8 like in human cancer
title_sort pan cancer analysis of the oncogenic role of n acetyltransferase 8 like in human cancer
topic Pan-cancer
Tumor immune microenvironment
Prognosis
N-Acetyltransferase 8 like
url https://doi.org/10.1007/s12672-024-01605-w
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