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HNF4G accelerates glioma progression by facilitating NRP1 transcription

  • Authors:
    • Hongmin Che
    • Qi Zheng
    • Zijun Liao
    • Lu Zhang
  • View Affiliations / Copyright

    Affiliations: Department of Neurosurgery, Xi'an Gaoxin Hospital, Xi'an, Shaanxi 710075, P.R. China, Department of Medical Oncology, Affiliated Shaanxi Provincial Cancer Hospital, College of Medicine, Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China, Department of Foreign Languages, Xi'an Mingde Institute of Technology, Xi'an, Shaanxi 710124, P.R. China
    Copyright: © Che et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 102
    |
    Published online on: February 1, 2023
       https://doi.org/10.3892/ol.2023.13688
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Abstract

Hepatocyte nuclear factor 4γ (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.
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Copy and paste a formatted citation
Spandidos Publications style
Che H, Zheng Q, Liao Z and Zhang L: HNF4G accelerates glioma progression by facilitating NRP1 transcription. Oncol Lett 25: 102, 2023.
APA
Che, H., Zheng, Q., Liao, Z., & Zhang, L. (2023). HNF4G accelerates glioma progression by facilitating NRP1 transcription. Oncology Letters, 25, 102. https://doi.org/10.3892/ol.2023.13688
MLA
Che, H., Zheng, Q., Liao, Z., Zhang, L."HNF4G accelerates glioma progression by facilitating NRP1 transcription". Oncology Letters 25.3 (2023): 102.
Chicago
Che, H., Zheng, Q., Liao, Z., Zhang, L."HNF4G accelerates glioma progression by facilitating NRP1 transcription". Oncology Letters 25, no. 3 (2023): 102. https://doi.org/10.3892/ol.2023.13688
Copy and paste a formatted citation
x
Spandidos Publications style
Che H, Zheng Q, Liao Z and Zhang L: HNF4G accelerates glioma progression by facilitating NRP1 transcription. Oncol Lett 25: 102, 2023.
APA
Che, H., Zheng, Q., Liao, Z., & Zhang, L. (2023). HNF4G accelerates glioma progression by facilitating NRP1 transcription. Oncology Letters, 25, 102. https://doi.org/10.3892/ol.2023.13688
MLA
Che, H., Zheng, Q., Liao, Z., Zhang, L."HNF4G accelerates glioma progression by facilitating NRP1 transcription". Oncology Letters 25.3 (2023): 102.
Chicago
Che, H., Zheng, Q., Liao, Z., Zhang, L."HNF4G accelerates glioma progression by facilitating NRP1 transcription". Oncology Letters 25, no. 3 (2023): 102. https://doi.org/10.3892/ol.2023.13688
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