HNF4G accelerates glioma progression by facilitating NRP1 transcription

Hepatocyte nuclear factor 4[gamma] (HNF4G) is considered to be a transcription factor and functions as an oncogene in certain types of human cancer. However, the precise functions and the potential molecular mechanisms of HNF4G in glioma remain unclear. Therefore, the present study aimed to elucidat...

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Bibliographic Details
Published in:Oncology letters 2023-03, Vol.25 (3), p.1, Article 102
Main Authors: Che, Hongmin, Zheng, Qi, Liao, Zijun, Zhang, Lu
Format: Article
Language:English
Subjects:
Analysis
Apoptosis
Brain cancer
Cell cycle
Cell growth
Chemotherapy
Development and progression
Gene expression
Genetic transcription
Glioma
Gliomas
Health aspects
Instrument industry
Laboratory animals
Patients
Plasmids
Radiation therapy
RNA
Scientific equipment and supplies industry
Tumors
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Summary:Hepatocyte nuclear factor 4[gamma] (HNF4G) is considered to be a transcription factor and functions as an oncogene in certain types of human cancer. However, the precise functions and the potential molecular mechanisms of HNF4G in glioma remain unclear. Therefore, the present study aimed to elucidate the role of HNF4G in glioma and the underlying mechanism. Western blotting and reverse transcription-quantitative PCR (RT-qPCR) demonstrated that HNF4G was highly expressed in glioma tissues and cell lines. The overexpression of HNF4G in LN229 and U251 glioma cells promoted cell proliferation and cell cycle progression, and inhibited apoptosis, while the knockdown of HNF4G suppressed cell proliferation, cell cycle progression and tumor growth, and induced apoptosis. A significant positive association was detected between HNF4G and neuropilin-1 (NRP1) mRNA expression in glioma tissues. Bioinformatics analysis, chromatin immunoprecipitation-RT-qPCR and promoter reporter assays confirmed that HNF4G promoted NRP1 transcription in glioma by binding to its promoter. NRP1 overexpression facilitated glioma cell proliferation and cell cycle progression, and suppressed apoptosis in vitro, while the knockdown of NRP1 inhibited cell proliferation and cell cycle progression, and facilitated apoptosis. NRP1 overexpression reversed the effects induced by HNF4G knockdown on glioma cell proliferation, cell cycle progression and apoptosis. In summary, the present study demonstrated that HNF4G promotes glioma cell proliferation and suppresses apoptosis by activating NRP1 transcription. These findings indicate that HNF4G acts as an oncogene in glioma and may thus be an effective therapeutic target for glioma. Key words: hepatocyte nuclear factor 4[gamma], neuropilin-1, glioma, proliferation, apoptosis
ISSN:1792-1074
1792-1082
DOI:10.3892/ol.2023.13688