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<p>Glioma is the most common primary malignant brain tumor globally, with a poor prognosis due to its complex interaction with the tumor microenvironment (TME). Despite advancements in glioma treatments, patient survival remains low, highlighting the need for additional molecular investigations. Long non-coding RNA Colorectal Neoplasia Differentially Expressed (lncRNA-CRNDE) has been linked to tumorigenesis in various cancers, influencing tumor progression via the tumor microenvironment (TME). Its role in tumor-associated macrophages in gliomas is unclear. This study investigates whether lncRNA-CRNDE promotes glioma progression by modulating these macrophages. Using the TCGA database, we assessed lncRNA-CRNDE expression and its prognostic significance in glioma, and its association with the immune microenvironment. We collected 42 glioma samples of different grades from our institution. Using RT-qPCR, Western blotting, ELISA, and other cell biology techniques, we analyzed lncRNA-CRNDE’s effects on glioma proliferation and invasion and validated its role in glioma progression through animal model experiments. TCGA bioinformatic analysis showed higher lncRNA-CRNDE expression in glioma than in normal tissues, which correlated with poorer prognosis. Clinical glioma samples via RT-qPCR also showed elevated lncRNA-CRNDE in tumors, which was associated with reduced survival. Cellular experiments confirmed lncRNA-CRNDE’s promotion of glioma proliferation and invasion, which was associated with the tumor microenvironment (TME). Further studies revealed lncRNA-CRNDE’s role in macrophage polarization in the TME, enhancing glioma progression. Animal experiments confirmed lncRNA-CRNDE’s role in glioma progression. LncRNA-CRNDE is highly expressed in M2 macrophages and strongly associated with glioma progression. It is a potential prognostic marker and therapeutic target for glioma.</p>

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Long Non-coding RNA CRNDE Promotes the Development of Glioma by Inducing Polarization of M2-Type Macrophages

  • 期刊论文

  • 发表日期：

    2025年5月5日

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  • Liang Sun,
  • Zhi Yang,
  • Haibin Chen,
  • Liwen Li,
  • Zhaohui Ying,
  • Yuanyuan Qu,
  • Nanyang Tong,
  • Liang Xia,
  • Caixing Sun

摘要

Glioma is the most common primary malignant brain tumor globally, with a poor prognosis due to its complex interaction with the tumor microenvironment (TME). Despite advancements in glioma treatments, patient survival remains low, highlighting the need for additional molecular investigations. Long non-coding RNA Colorectal Neoplasia Differentially Expressed (lncRNA-CRNDE) has been linked to tumorigenesis in various cancers, influencing tumor progression via the tumor microenvironment (TME). Its role in tumor-associated macrophages in gliomas is unclear. This study investigates whether lncRNA-CRNDE promotes glioma progression by modulating these macrophages. Using the TCGA database, we assessed lncRNA-CRNDE expression and its prognostic significance in glioma, and its association with the immune microenvironment. We collected 42 glioma samples of different grades from our institution. Using RT-qPCR, Western blotting, ELISA, and other cell biology techniques, we analyzed lncRNA-CRNDE’s effects on glioma proliferation and invasion and validated its role in glioma progression through animal model experiments. TCGA bioinformatic analysis showed higher lncRNA-CRNDE expression in glioma than in normal tissues, which correlated with poorer prognosis. Clinical glioma samples via RT-qPCR also showed elevated lncRNA-CRNDE in tumors, which was associated with reduced survival. Cellular experiments confirmed lncRNA-CRNDE’s promotion of glioma proliferation and invasion, which was associated with the tumor microenvironment (TME). Further studies revealed lncRNA-CRNDE’s role in macrophage polarization in the TME, enhancing glioma progression. Animal experiments confirmed lncRNA-CRNDE’s role in glioma progression. LncRNA-CRNDE is highly expressed in M2 macrophages and strongly associated with glioma progression. It is a potential prognostic marker and therapeutic target for glioma.