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Increased PYCR1 mRNA predicts poor prognosis in kidney adenocarcinoma: A study based on TCGA database.

Authors :
Zhang T
Liu Y
Liu W
Li Q
Hou W
Huang Y
Lv P
Meng L
Li Y
Jia Y
Liu X
Zuo Z
Source :
Medicine [Medicine (Baltimore)] 2021 Sep 24; Vol. 100 (38), pp. e27145.
Publication Year :
2021

Abstract

Abstract: The pyrroline-5-carboxylate reductase 1 (PYCR1) plays important roles in cancers, but its contribution to adenocarcinoma of the kidney (AK) and the potential mechanism remain to be clarified. In this study, we aimed to demonstrate the relationship between PYCR1 mRNA and AK based on The Cancer Genome Atlas database.PYCR1 mRNA in AK and normal tissues was compared using Wilcoxon rank sum test. The relationship between PYCR1 mRNA and clinicopathological characters was evaluated using logistic regression. The association between PYCR1 mRNA and survival rate was evaluated using Kaplan-Meier test and Cox regression of univariate and multivariate analysis. Additionally, Gene Set Enrichment Analysis was conducted to annotate the biological function of PYCR1 mRNA.Increased PYCR1 mRNA was found in AK tissues. Increased PYCR1 mRNA was related to high histologic grade, clinical stage, and lymph node and distant metastasis. Kaplan-Meier survival analysis and univariate analysis showed that AK patients with increased PYCR1 mRNA had worse prognosis than those without. PYCR1 mRNA remained independently associated with overall survival (HR: 1.34; 95% CI: 1.07-1.66; Pā€Š=ā€Š.009) in multivariate analysis. The Gene Set Enrichment Analysis suggested that ribosome, proteasome, inhibition of p53 signaling pathway, extracellular matrix receptor interaction, and homologous recombination were differentially enriched in increased PYCR1 mRNA phenotype.Increased PYCR1 mRNA is a potential marker in patients with AK. More importantly, p53 pathway, ribosome, proteasome, extracellular matrix receptor interaction, and homologous are differentially enriched in AK patients with increased PYCR1 mRNA.<br />Competing Interests: The authors have no conflicts of interest to disclose.<br /> (Copyright © 2021 the Author(s). Published by Wolters Kluwer Health, Inc.)

Details

Language :
English
ISSN :
1536-5964
Volume :
100
Issue :
38
Database :
MEDLINE
Journal :
Medicine
Publication Type :
Academic Journal
Accession number :
34559102
Full Text :
https://doi.org/10.1097/MD.0000000000027145