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A novel lipid metabolism gene signature for clear cell renal cell carcinoma using integrated bioinformatics analysis

Background: Clear cell renal cell carcinoma (ccRCC), which is the most prevalent type of renal cell carcinoma, has a high mortality rate. Lipid metabolism reprogramming is a hallmark of ccRCC progression, but its specific mechanism remains unclear. Here, the relationship between dysregulated lipid m...

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Autores principales: Li, Ke, Zhu, Yan, Cheng, Jiawei, Li, Anlei, Liu, Yuxing, Yang, Xinyi, Huang, Hao, Peng, Zhangzhe, Xu, Hui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9971983/
https://www.ncbi.nlm.nih.gov/pubmed/36866272
http://dx.doi.org/10.3389/fcell.2023.1078759
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author Li, Ke
Zhu, Yan
Cheng, Jiawei
Li, Anlei
Liu, Yuxing
Yang, Xinyi
Huang, Hao
Peng, Zhangzhe
Xu, Hui
author_facet Li, Ke
Zhu, Yan
Cheng, Jiawei
Li, Anlei
Liu, Yuxing
Yang, Xinyi
Huang, Hao
Peng, Zhangzhe
Xu, Hui
author_sort Li, Ke
collection PubMed
description Background: Clear cell renal cell carcinoma (ccRCC), which is the most prevalent type of renal cell carcinoma, has a high mortality rate. Lipid metabolism reprogramming is a hallmark of ccRCC progression, but its specific mechanism remains unclear. Here, the relationship between dysregulated lipid metabolism genes (LMGs) and ccRCC progression was investigated. Methods: The ccRCC transcriptome data and patients’ clinical traits were obtained from several databases. A list of LMGs was selected, differentially expressed gene screening performed to detect differential LMGs, survival analysis performed, a prognostic model established, and immune landscape evaluated using the CIBERSORT algorithm. Gene Set Variation Analysis and Gene set enrichment analysis were conducted to explore the mechanism by which LMGs affect ccRCC progression. Single-cell RNA-sequencing data were obtained from relevant datasets. Immunohistochemistry and RT-PCR were used to validate the expression of prognostic LMGs. Results: Seventy-one differential LMGs were identified between ccRCC and control samples, and a novel risk score model established comprising 11 LMGs (ABCB4, DPEP1, IL4I1, ENO2, PLD4, CEL, HSD11B2, ACADSB, ELOVL2, LPA, and PIK3R6); this risk model could predict ccRCC survival. The high-risk group had worse prognoses and higher immune pathway activation and cancer development. Conclusion: Our results showed that this prognostic model can affect ccRCC progression.
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spelling pubmed-99719832023-03-01 A novel lipid metabolism gene signature for clear cell renal cell carcinoma using integrated bioinformatics analysis Li, Ke Zhu, Yan Cheng, Jiawei Li, Anlei Liu, Yuxing Yang, Xinyi Huang, Hao Peng, Zhangzhe Xu, Hui Front Cell Dev Biol Cell and Developmental Biology Background: Clear cell renal cell carcinoma (ccRCC), which is the most prevalent type of renal cell carcinoma, has a high mortality rate. Lipid metabolism reprogramming is a hallmark of ccRCC progression, but its specific mechanism remains unclear. Here, the relationship between dysregulated lipid metabolism genes (LMGs) and ccRCC progression was investigated. Methods: The ccRCC transcriptome data and patients’ clinical traits were obtained from several databases. A list of LMGs was selected, differentially expressed gene screening performed to detect differential LMGs, survival analysis performed, a prognostic model established, and immune landscape evaluated using the CIBERSORT algorithm. Gene Set Variation Analysis and Gene set enrichment analysis were conducted to explore the mechanism by which LMGs affect ccRCC progression. Single-cell RNA-sequencing data were obtained from relevant datasets. Immunohistochemistry and RT-PCR were used to validate the expression of prognostic LMGs. Results: Seventy-one differential LMGs were identified between ccRCC and control samples, and a novel risk score model established comprising 11 LMGs (ABCB4, DPEP1, IL4I1, ENO2, PLD4, CEL, HSD11B2, ACADSB, ELOVL2, LPA, and PIK3R6); this risk model could predict ccRCC survival. The high-risk group had worse prognoses and higher immune pathway activation and cancer development. Conclusion: Our results showed that this prognostic model can affect ccRCC progression. Frontiers Media S.A. 2023-02-14 /pmc/articles/PMC9971983/ /pubmed/36866272 http://dx.doi.org/10.3389/fcell.2023.1078759 Text en Copyright © 2023 Li, Zhu, Cheng, Li, Liu, Yang, Huang, Peng and Xu. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Cell and Developmental Biology
Li, Ke
Zhu, Yan
Cheng, Jiawei
Li, Anlei
Liu, Yuxing
Yang, Xinyi
Huang, Hao
Peng, Zhangzhe
Xu, Hui
A novel lipid metabolism gene signature for clear cell renal cell carcinoma using integrated bioinformatics analysis
title A novel lipid metabolism gene signature for clear cell renal cell carcinoma using integrated bioinformatics analysis
title_full A novel lipid metabolism gene signature for clear cell renal cell carcinoma using integrated bioinformatics analysis
title_fullStr A novel lipid metabolism gene signature for clear cell renal cell carcinoma using integrated bioinformatics analysis
title_full_unstemmed A novel lipid metabolism gene signature for clear cell renal cell carcinoma using integrated bioinformatics analysis
title_short A novel lipid metabolism gene signature for clear cell renal cell carcinoma using integrated bioinformatics analysis
title_sort novel lipid metabolism gene signature for clear cell renal cell carcinoma using integrated bioinformatics analysis
topic Cell and Developmental Biology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9971983/
https://www.ncbi.nlm.nih.gov/pubmed/36866272
http://dx.doi.org/10.3389/fcell.2023.1078759
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