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Background <p>Nuclear factor IX (NFIX) promotes glioblastoma (GBM) development by inducing GBM cell migration and proliferation. However, the upstream regulatory mechanisms of NFIX in GBM remain unclear.</p> Methods and results <p>To investigate the functional role of miR-1270 in GBM, a stable miR-1270-overexpressing cell model was constructed using lentiviral transduction. The functional consequences were systematically evaluated using Transwell migration, colony formation, and CCK-8 assays, as well as western blotting and quantitative real-time polymerase chain reaction. To validate the therapeutic potential in vivo, we established orthotopic xenograft models in nude mice and longitudinally monitored tumor progression through non-invasive small animal imaging, enabling comprehensive assessment of the antitumor effects of miR-1270 within a physiological microenvironment. A decrease in microRNA-1270 (miR-1270) expression in human GBM samples was observed, which was negatively correlated with NFIX expression. The miR-1270 inhibited NFIX expression, a key driver of GBM cell proliferation and migration. Mechanistic analysis revealed that miR-1270 directly bound to the NFIX promoter region, suppressing its transcriptional activity. The reintroduction of NFIX counteracted the inhibitory effects of miR-1270 on GBM cell malignancy.</p> Conclusions <p>This study is the first to report the transcriptional inhibition of NFIX by miR-1270 in GBM cells. These findings suggest that targeting the miR-1270–NFIX axis may provide a promising therapeutic strategy for GBM.</p>

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miR-1270 suppresses glioblastoma development by transcriptional inhibition of nuclear factor IX

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月15日

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  • Zhengwei Wang,
  • Jiani Lin,
  • Guisen Tan,
  • Tingzheng Pan,
  • Hongtian Zhang,
  • Jiangang Liu

摘要

Background

Nuclear factor IX (NFIX) promotes glioblastoma (GBM) development by inducing GBM cell migration and proliferation. However, the upstream regulatory mechanisms of NFIX in GBM remain unclear.

Methods and results

To investigate the functional role of miR-1270 in GBM, a stable miR-1270-overexpressing cell model was constructed using lentiviral transduction. The functional consequences were systematically evaluated using Transwell migration, colony formation, and CCK-8 assays, as well as western blotting and quantitative real-time polymerase chain reaction. To validate the therapeutic potential in vivo, we established orthotopic xenograft models in nude mice and longitudinally monitored tumor progression through non-invasive small animal imaging, enabling comprehensive assessment of the antitumor effects of miR-1270 within a physiological microenvironment. A decrease in microRNA-1270 (miR-1270) expression in human GBM samples was observed, which was negatively correlated with NFIX expression. The miR-1270 inhibited NFIX expression, a key driver of GBM cell proliferation and migration. Mechanistic analysis revealed that miR-1270 directly bound to the NFIX promoter region, suppressing its transcriptional activity. The reintroduction of NFIX counteracted the inhibitory effects of miR-1270 on GBM cell malignancy.

Conclusions

This study is the first to report the transcriptional inhibition of NFIX by miR-1270 in GBM cells. These findings suggest that targeting the miR-1270–NFIX axis may provide a promising therapeutic strategy for GBM.