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<p>Gliomas are the most lethal primary brain tumors with poor survival and high recurrence. The role of long non-coding RNA <i>FOXP4</i> antisense RNA 1 (lncRNA <i>FOXP4-AS1</i>) in glioma progression remains largely unknown. This study aimed to evaluate the clinical significance of <i>FOXP4-AS1</i> in glioma and to elucidate its functional role and molecular mechanisms. <i>FOXP4-AS1</i> expression was measured in 113 glioma tissues by reverse transcription-quantitative PCR (RT-qPCR) and correlated with clinicopathological features. In vitro functional assays, including Cell Counting Kit-8 (CCK-8), Transwell, apoptosis detection, and glycolysis evaluation, were performed following <i>FOXP4-AS1</i> knockdown. Bioinformatics predictions and dual-luciferase reporter assays were used to validate the interaction among <i>FOXP4-AS1</i>, microRNA‑136‑5p (miR‑136‑5p), and ADCYAP receptor type I (<i>ADCYAP1R1</i>). <i>FOXP4-AS1</i> was upregulated in glioma and correlated with higher World Health Organization (WHO) grade (III–IV), larger tumor size, and lower Karnofsky Performance Status (KPS) score, indicating aggressive progression and poor prognosis. Knockdown of <i>FOXP4-AS1</i> inhibited glioma cell proliferation, migration, invasion, and glycolysis, while promoting apoptosis. Mechanistically, <i>FOXP4-AS1</i> acted as a molecular sponge for miR‑136‑5p, thereby upregulating <i>ADCYAP1R1</i> expression. Rescue experiments demonstrated that <i>FOXP4-AS1</i> promotes glioma progression by sponging miR‑136‑5p and that miR‑136‑5p suppresses tumor growth by targeting <i>ADCYAP1R1</i>, as shown by reversed phenotypes upon miR‑136‑5p inhibition or <i>ADCYAP1R1</i> overexpression. These findings demonstrate that <i>FOXP4-AS1</i> promotes glioma progression via the miR‑136‑5p/<i>ADCYAP1R1</i> axis, highlighting its potential as a prognostic biomarker and therapeutic target in glioma.</p>

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LncRNA FOXP4-AS1 promotes glioma cell proliferation, metastasis, and glycolysis via the miR-136-5p/ADCYAP1R1 axis

  • 期刊论文

  • 发表日期：

    2026年3月7日

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  • Jun Wang,
  • Minshen Wang,
  • Qiufeng Dong,
  • Junli Huo,
  • Zhifeng Yan,
  • Juan Li,
  • Xiaoyan Chen,
  • Liwen Li,
  • Haining Zhen

摘要

Gliomas are the most lethal primary brain tumors with poor survival and high recurrence. The role of long non-coding RNA FOXP4 antisense RNA 1 (lncRNA FOXP4-AS1) in glioma progression remains largely unknown. This study aimed to evaluate the clinical significance of FOXP4-AS1 in glioma and to elucidate its functional role and molecular mechanisms. FOXP4-AS1 expression was measured in 113 glioma tissues by reverse transcription-quantitative PCR (RT-qPCR) and correlated with clinicopathological features. In vitro functional assays, including Cell Counting Kit-8 (CCK-8), Transwell, apoptosis detection, and glycolysis evaluation, were performed following FOXP4-AS1 knockdown. Bioinformatics predictions and dual-luciferase reporter assays were used to validate the interaction among FOXP4-AS1, microRNA‑136‑5p (miR‑136‑5p), and ADCYAP receptor type I (ADCYAP1R1). FOXP4-AS1 was upregulated in glioma and correlated with higher World Health Organization (WHO) grade (III–IV), larger tumor size, and lower Karnofsky Performance Status (KPS) score, indicating aggressive progression and poor prognosis. Knockdown of FOXP4-AS1 inhibited glioma cell proliferation, migration, invasion, and glycolysis, while promoting apoptosis. Mechanistically, FOXP4-AS1 acted as a molecular sponge for miR‑136‑5p, thereby upregulating ADCYAP1R1 expression. Rescue experiments demonstrated that FOXP4-AS1 promotes glioma progression by sponging miR‑136‑5p and that miR‑136‑5p suppresses tumor growth by targeting ADCYAP1R1, as shown by reversed phenotypes upon miR‑136‑5p inhibition or ADCYAP1R1 overexpression. These findings demonstrate that FOXP4-AS1 promotes glioma progression via the miR‑136‑5p/ADCYAP1R1 axis, highlighting its potential as a prognostic biomarker and therapeutic target in glioma.