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<p>Recent studies have demonstrated that <i>PLEKHA4</i> promotes tumor growth in some cancers, such as small-cell lung cancer, melanoma, and hepatic carcinomas; however, the underlying mechanism in glioblastoma remains ambiguous. Bioinformatic was used to analysis <i>PLEKHA4</i> expression. In vitro and in vivo experiments were conducted to detect the effect of <i>PLEKHA4</i> on glioblastoma cell glycolytic reprogramming and progression. GSEA was used to analyze the signal pathways related to <i>PLEKHA4</i>. Pharmacological methods further validated the role of activation pathways. We evaluated the effects of <i>PLEKHA4</i> knockdown combined with temozolomide (TMZ) on glioblastoma cell proliferation and apoptosis in vitro and in vivo. We observed an overexpression of <i>PLEKHA4</i> in GBM cell lines, resulting in enhanced cell proliferation, inhibited apoptosis, and promoted glycolysis. Mechanistically, our study demonstrated that <i>PLEKHA4</i> mediates cell proliferation, apoptosis, and glycolysis via the <i>STAT3/SOCS1</i> signaling pathway. Additionally, <i>HOXD9</i> was predicted using Jasper, which is a transcription factor that binds to the <i>PLEKHA4</i> promoter region. Knocking down <i>PLEKHA4</i> combined with TMZ inhibited cell proliferation and promoted cell apoptosis in vitro and in vivo. Our results indicated that <i>HOXD9</i>-medicated <i>PLEKHA4</i> regulates glioblastoma cell proliferation and glycolysis via activation of the <i>STAT3/SOCS1</i> pathway.</p>

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PLEKHA4 is transcriptionally regulated by HOXD9 and regulates glycolytic reprogramming and progression in glioblastoma via activation of the STAT3/SOCS-1 pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年5月9日

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  • Dainan Zhang,
  • Xiaoyin Wang,
  • Meng Xiao,
  • Shunchang Ma,
  • Shaomin Li,
  • Wang Jia

摘要

Recent studies have demonstrated that PLEKHA4 promotes tumor growth in some cancers, such as small-cell lung cancer, melanoma, and hepatic carcinomas; however, the underlying mechanism in glioblastoma remains ambiguous. Bioinformatic was used to analysis PLEKHA4 expression. In vitro and in vivo experiments were conducted to detect the effect of PLEKHA4 on glioblastoma cell glycolytic reprogramming and progression. GSEA was used to analyze the signal pathways related to PLEKHA4. Pharmacological methods further validated the role of activation pathways. We evaluated the effects of PLEKHA4 knockdown combined with temozolomide (TMZ) on glioblastoma cell proliferation and apoptosis in vitro and in vivo. We observed an overexpression of PLEKHA4 in GBM cell lines, resulting in enhanced cell proliferation, inhibited apoptosis, and promoted glycolysis. Mechanistically, our study demonstrated that PLEKHA4 mediates cell proliferation, apoptosis, and glycolysis via the STAT3/SOCS1 signaling pathway. Additionally, HOXD9 was predicted using Jasper, which is a transcription factor that binds to the PLEKHA4 promoter region. Knocking down PLEKHA4 combined with TMZ inhibited cell proliferation and promoted cell apoptosis in vitro and in vivo. Our results indicated that HOXD9-medicated PLEKHA4 regulates glioblastoma cell proliferation and glycolysis via activation of the STAT3/SOCS1 pathway.