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利用生物信息学策略探索膀胱癌中与FGFR3相关的致癌机制。

Exploring the FGFR3-related oncogenic mechanism in bladder cancer using bioinformatics strategy.

作者信息

Cao Wei, Ma Enguang, Zhou Li, Yuan Tan, Zhang Chunying

机构信息

Department of Urinary Surgery, The Second Affiliated Hospital of Harbin Medical University, 150086, Harbin, Heilongjiang province, China.

Department of Urinary Surgery, Harbin First Hospital, 150010, Harbin, Heilongjiang province, China.

出版信息

World J Surg Oncol. 2017 Mar 20;15(1):66. doi: 10.1186/s12957-017-1125-4.

DOI:10.1186/s12957-017-1125-4
PMID:28320388
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5359882/
Abstract

BACKGROUND

Aberrant activation of fibroblast growth factor receptor 3 (FGFR3) is frequently observed in bladder cancer, but how it involved in carcinogenesis is not well understood. The current study was aimed to investigate the underlying mechanism on the progression of bladder cancer.

METHODS

The GSE41035 dataset downloaded from Gene Expression Omnibus was used to identify the differentially expressed genes (DEGs) between bladder cancer cell line RT112 with or without depletion of FGFR3, and gene ontology enrichment analysis was performed. Then, FGFR3-centered protein-protein interaction (PPI) and regulatory networks were constructed. Combined with the data retrieved from GSE31684, prognostic makers for bladder cancer were predicted.

RESULTS

We identified a total of 2855 DEGs, and most of them were associated with blood vessel morphogenesis and cell division. In addition, KIAA1377, POLA2, FGFR3, and EPHA4 were the hub genes with high degree in the FGFR3-centered PPI network. Besides, 17 microRNAs (miRNAs) and 6 transcriptional factors (TFs) were predicted to be the regulators of the nodes in PPI network. Moreover, CSTF2, POLA1, HMOX2, and EFNB2 may be associated with the prognosis of bladder cancer patient.

CONCLUSIONS

The current study may provide some insights into the molecular mechanism of FGFR3 as a mediator in bladder cancer.

摘要

背景

成纤维细胞生长因子受体3(FGFR3)的异常激活在膀胱癌中经常被观察到,但其在致癌过程中的作用机制尚不清楚。本研究旨在探讨膀胱癌进展的潜在机制。

方法

使用从基因表达综合数据库下载的GSE41035数据集,鉴定FGFR3缺失或未缺失的膀胱癌细胞系RT112之间的差异表达基因(DEG),并进行基因本体富集分析。然后,构建以FGFR3为中心的蛋白质-蛋白质相互作用(PPI)和调控网络。结合从GSE31684检索到的数据,预测膀胱癌的预后标志物。

结果

我们共鉴定出2855个DEG,其中大多数与血管形态发生和细胞分裂相关。此外,KIAA1377、POLA2、FGFR3和EPHA4是FGFR3为中心的PPI网络中度数较高的枢纽基因。此外,预测17种微小RNA(miRNA)和6种转录因子(TF)是PPI网络中节点的调节因子。此外,CSTF2、POLA1、HMOX2和EFNB2可能与膀胱癌患者的预后有关。

结论

本研究可能为FGFR3作为膀胱癌中介物的分子机制提供一些见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6504/5359882/f5d62937814e/12957_2017_1125_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6504/5359882/ffe833ef0e8e/12957_2017_1125_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6504/5359882/8433e1279f39/12957_2017_1125_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6504/5359882/f5d62937814e/12957_2017_1125_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6504/5359882/ffe833ef0e8e/12957_2017_1125_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6504/5359882/8433e1279f39/12957_2017_1125_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6504/5359882/f5d62937814e/12957_2017_1125_Fig3_HTML.jpg

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