Down-Regulation of Phosphoribosyl Pyrophosphate Synthetase 1 Inhibits Neuroblastoma Cell Proliferation.

Jifu Li,Shunqin Zhu,Hongjuan Cui,Junhong Ye

doi:10.3390/cells8090955

Jifu Li, Shunqin Zhu + Show 2 more

Open Access

https://doi.org/10.3390/cells8090955

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Journal: Cells	Publication Date: Aug 22, 2019
Citations: 11	License type: CC BY 4.0

Affiliation: Southwest University

Abstract

Phosphoribosyl pyrophosphate synthetase 1 (PRPS1) is a key enzyme in de novo nucleotide synthesis and nucleotide salvage synthesis pathways that are critical for purine and pyrimidine biosynthesis. Abnormally high expression of PRPS1 can cause many diseases, including hearing loss, hypotonia, and ataxia, in addition to being associated with neuroblastoma. However, the role of PRPS1 in neuroblastoma is still unclear. In this study, we found that PRPS1 was commonly expressed in neuroblastoma cells and was closely related to poor prognosis for cancer. Furthermore, down-regulation of PRPS1 inhibited neuroblastoma cell proliferation and tumor growth in vitro and in vivo via disturbing DNA synthesis. This study provides new insights into the treatment of neuroblastoma patients and new targets for drug development.

Highlights

Neuroblastoma is one of the most common types of solid tumor and exhibits high malignancy rates in children [1,2,3,4]
To investigate whether pyrophosphate synthetase 1 (PRPS1) is associated with neuroblastoma patient prognosis, a Kaplan–Meier analysis based on the R2 database was first conducted
We determined that PRPS1 expression was a potential prognostic marker in neuroblastoma patients

Summary

Introduction

Neuroblastoma is one of the most common types of solid tumor and exhibits high malignancy rates in children [1,2,3,4]. Neuroblastoma has a poor prognosis, metastasizes, recurs frequently, and is very heterogeneous [6,7,8]. Neuroblastoma can be divided into three types based on the degree of differentiation: undifferentiated, poorly differentiated, and differentiated. A small number of neuroblastoma cases can transform into benign tumors spontaneously with little or no systemic treatment. Neuroblastoma is self-regressing and differentiates in vitro, rendering it a good tumor model to understand the mechanisms of cancer cell proliferation and differentiation and identify new strategies for clinical treatment [6,9,10,11]

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