Abstract

We explored the difference in expression of tubulin alpha 1b (TUBA1B) between Wilms' tumor (WT) and normal tissues (NT) from in-house patients and databases, to determine TUBA1B expression in WT and the predictive pathways of coexpressed genes. In-house RNA-sequencing data were performed with WT and NT from three patients from our institute. Other four RNA-sequencing and microarray data were also downloaded from multiple public databases. The TUBA1B expression between WT and NT was analyzed by Student's t-test and meta-analysis. The correlation between the expression of TUBA1B and other genes in each study was analyzed. Genes with p < 0.05 and r > 0.5 were considered as the coexpressing genes of TUBA1B. Overlapping the coexpressed genes of the five studies, including three in-house patients (3 WT vs. 3 NT), GTEx-TARGET (126 WT vs. 51 NT), GSE2172 (18 WT vs. 3 NT), GSE11024 (27 WT vs. 12 NT), and GSE73209 (32 WT vs. 6 NT), were performed with limma and VennDiagram packages in R software. The website of WEB-based GEne SeT AnaLysis toolkit were used to analyze the gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional annotations for the overlapped genes. The results showed that the relative expression of TUBA1B in WT tissues from in-house three patients was 280.0086, 141.7589, and 303.8292 and that in NT was 16.5836, 104.8141, and 12.79 (3 WT vs. 3 NT, p = 0.0285, ROC = 100%, SMD = 2.74). Student's t-test and meta-analysis in all studies revealed that the expression of TUBA1B was upregulated in WT tissues compared to that in NT (p < 0.05, SMD = 2.89, sROC = 0.98). Finally, the research identified the expression of TUBA1B in WT tissues was significantly upregulated than that in NT. The coexpressed genes of TUBA1B were enriched in the pathway of DNA replication, mismatch repair, cell cycle, pathogenic Escherichia coli infection, and spliceosome.

Highlights

  • Wilms’ tumor (WT), called nephroblastoma, usually originates from embryonic renal precursor cells in which the cell growth and/or differentiation is dysregulated during development

  • This was the first study to report that the expression of TUBA1B in the WT tissues was higher than that in the NT, indicating that TUBA1B might play an essential role in WT

  • In order to explore the possible ways in which TUBA1B may influence WT, we obtained 80 coexpression genes and its KEGG enrichment analysis

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Summary

Introduction

Wilms’ tumor (WT), called nephroblastoma, usually originates from embryonic renal precursor cells in which the cell growth and/or differentiation is dysregulated during development. It accounts for 90% of childhood renal tumors and constitutes 7% of all childhood cancers and is the commonest species of kidney tumor in childhood with an annual incidence of 8–10 per million. The molecular mechanism of various types of tumor development has gradually become clear. The molecular mechanisms underlying the development of solid tumors in children have been investigated to a lesser extent. WT lacks specific tumor markers; it is even more important to clarify the pathogenesis of malignant tumors in children, BioMed Research International

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