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High expression of HOXA4 in patients with glioma indicates unfavorable clinical outcomes

Authors :
Zhenghong Yu
Zhendong Liu
Xiaoyu Lian
Xingbo Cheng
Binfeng Liu
Bo Zhang
Hongbo Wang
Jialin Wang
Ang Li
Zhishuai Ren
Bo Pang
Rongjun Qian
Yanzheng Gao
Source :
Cell Cycle. 21:2387-2402
Publication Year :
2022
Publisher :
Informa UK Limited, 2022.

Abstract

iHOXA4/iis a novel oncogene that has been observed in many kinds of tumors, but its role during glioma carcinogenesis and its clinical significance in diagnosing and prognosis human glioma remains unknown. In the present study, the Chinese Glioma Atlas (CGGA)-RNA sequencing database, CGGA microarray, and The Cancer Genome Atlas (TCGA)-RNA seq data from 1674 glioma patients were obtained from online databases and analyzed using quantitative reverse transcription-polymerase chain reaction (RT-qPCR) to detect changes in the expression level ofiHOXA4/iand characterize the relationship betweeniHOXA4/iand the clinical characteristics and prognosis of patients with glioma. Gene set enrichment analysis (GSEA) was used to reveal howiHOXA4/iregulates tumor-related pathways.iHOXA4/imRNA levels in glioma tissue were higher than those in adjacent brain tissue.iHOXA4/iexpression was also closely related to the clinical and molecular characteristics of gliomas, such as tumor grade and isocitrate dehydrogenase (IDH) mutation. Functional enrichment analysis revealed thatiHOXA4/icould regulate cancer-related signal pathways, such as Cell cycle, Cell adhesion molecules cams, and JAK/STAT signaling pathway. Results ofiin vitro/iexperiments confirmed that knockdown of HOXA4 blocks the cell cycle pathway and inhibits the proliferation, invasion and chemotherapy resistance in gliomas. We concluded thatiHOXA4/iwas an independent risk factor for glioma and may have clinical diagnostic potential. Meanwhile, our findings revealed thatiHOXA4/icould be used as a biomarker for glioma diagnosis and treatment.

Details

ISSN :
15514005 and 15384101
Volume :
21
Database :
OpenAIRE
Journal :
Cell Cycle
Accession number :
edsair.doi.dedup.....7200ee1a62e2134631e8e3ea6a704349