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Introduction <p>Gliomas present formidable challenges due to their aggressive nature and limited treatment efficacy. This study examines the roles of circFAT1(e2) and the <i>MYB</i> gene family, particularly <i>MYBL2</i>, in glioma etiology.</p> Materials and methods <p>Functional experiments were conducted to investigate the impact of MYBL2 on glioma cell behavior. Techniques such as quantitative polymerase chain reaction (qPCR), Western blotting (WB), Flow cytometry assays, cell counting Kit-8 (CCK-8), Transwell assays, colony formation assays as well as in vivo tumor growth were employed. Additionally, luciferase assays and RNA interference techniques were employed to investigate the regulatory relationship between miR-30e-5p, MYBL2, and circFAT1 (e2).</p> Results <p>Different expression patterns of the <i>MYB</i> gene family were observed in glioma subtypes, with <i>MYBL2</i> emerging as a predictive biomarker. A nomogram combining <i>MYBL2</i> expression and patient age predicted survival, negatively correlating with increased <i>MYBL2</i> expression. <i>MYBL2</i> knockdown affects glioma cell migration, invasion, and proliferation, suggesting its tumorigenic role. miR-30e-5p was identified as a direct regulator of <i>MYBL2</i>, decreasing its levels and suppressing glioma growth upon overexpression. Additionally, circFAT1(e2) was found to be predominantly cytoplasmic, resistant to RNase R, and stable as circular RNA. Silencing circFAT1(e2) reduced glioma growth and metastasis, inducing G1 phase cell cycle arrest. Conversely, circFAT1(e2) overexpression countered apoptosis induced by miR-30e-5p mimics.</p> Conclusions <p>This study unveils a regulatory axis involving miR-30e-5p, circFAT1(e2), and <i>MYBL2</i>, offering potential therapeutic targets for glioma treatment and shedding light on its molecular complexity.</p>

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CircFAT1(e2) acts as a sponge for miR-30e-5p and inhibits glioma progression by regulating MYBL2-mediated cell proliferation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月24日

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  • Zengjin Liu,
  • Shewei Guo,
  • Yahui Bai,
  • Zhenyu Song

摘要

Introduction

Gliomas present formidable challenges due to their aggressive nature and limited treatment efficacy. This study examines the roles of circFAT1(e2) and the MYB gene family, particularly MYBL2, in glioma etiology.

Materials and methods

Functional experiments were conducted to investigate the impact of MYBL2 on glioma cell behavior. Techniques such as quantitative polymerase chain reaction (qPCR), Western blotting (WB), Flow cytometry assays, cell counting Kit-8 (CCK-8), Transwell assays, colony formation assays as well as in vivo tumor growth were employed. Additionally, luciferase assays and RNA interference techniques were employed to investigate the regulatory relationship between miR-30e-5p, MYBL2, and circFAT1 (e2).

Results

Different expression patterns of the MYB gene family were observed in glioma subtypes, with MYBL2 emerging as a predictive biomarker. A nomogram combining MYBL2 expression and patient age predicted survival, negatively correlating with increased MYBL2 expression. MYBL2 knockdown affects glioma cell migration, invasion, and proliferation, suggesting its tumorigenic role. miR-30e-5p was identified as a direct regulator of MYBL2, decreasing its levels and suppressing glioma growth upon overexpression. Additionally, circFAT1(e2) was found to be predominantly cytoplasmic, resistant to RNase R, and stable as circular RNA. Silencing circFAT1(e2) reduced glioma growth and metastasis, inducing G1 phase cell cycle arrest. Conversely, circFAT1(e2) overexpression countered apoptosis induced by miR-30e-5p mimics.

Conclusions

This study unveils a regulatory axis involving miR-30e-5p, circFAT1(e2), and MYBL2, offering potential therapeutic targets for glioma treatment and shedding light on its molecular complexity.