ArticleFunctional & integrative genomics2026
LncRNA FOXP4-AS1 promotes glioma cell proliferation, metastasis, and glycolysis via the miR-136-5p/ADCYAP1R1 axis.
Article in Functional & integrative genomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- A cuproptosis-related lncRNAs-based risk signature for predicting prognosis and immune status in glioma.Translational cancer research · 2026Article
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9 authors.
Funding
Abstract
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.
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