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Purpose <p>This study aimed to investigate the characteristics and functional role of macrophage(MΦ)-glioma hybrid cells formed through cell fusion, and to explore the underlying mechanisms and potential therapeutic targets in glioma progression.</p> Methods <p>The presence of MΦ-glioma double-positive cells was confirmed using single-cell sequencing data and human glioma specimens. An in vitro fusion model was established, and hybrid cells were analyzed for flow cytometry. Functional assays assessed proliferation and invasion capabilities. Mechanistic studies focused on the role of SLC7A5, a MΦ-derived gene, and drug sensitivity was tested using the SLC7A5 inhibitor JPH203.</p> Results <p>MΦ-glioma hybrid cells were identified both in vivo and in vitro. These hybrids exhibited increased chromosomal content and demonstrated significantly enhanced proliferation and invasion. Mechanistically, SLC7A5 was identified as a key driver of this malignant phenotype. Furthermore, hybrid cells showed greater sensitivity to the SLC7A5 inhibitor JPH203 compared to parental cells.</p> Conclusion <p>Fusion with MΦs confers enhanced malignancy to glioma cells, characterized by increased proliferation and invasion, which is promoted by the MΦ-derived gene SLC7A5. Targeting SLC7A5 represents a promising novel therapeutic strategy for glioma.</p>

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Glioma cells achieve malignant progression by fusion with macrophages to gain high SLC7A5 expression

  • 期刊论文

  • 发表日期：

    2025年12月16日

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  • Yuedong Hu,
  • Fusheng Liu,
  • Ruifang Mi

摘要

Purpose

This study aimed to investigate the characteristics and functional role of macrophage(MΦ)-glioma hybrid cells formed through cell fusion, and to explore the underlying mechanisms and potential therapeutic targets in glioma progression.

Methods

The presence of MΦ-glioma double-positive cells was confirmed using single-cell sequencing data and human glioma specimens. An in vitro fusion model was established, and hybrid cells were analyzed for flow cytometry. Functional assays assessed proliferation and invasion capabilities. Mechanistic studies focused on the role of SLC7A5, a MΦ-derived gene, and drug sensitivity was tested using the SLC7A5 inhibitor JPH203.

Results

MΦ-glioma hybrid cells were identified both in vivo and in vitro. These hybrids exhibited increased chromosomal content and demonstrated significantly enhanced proliferation and invasion. Mechanistically, SLC7A5 was identified as a key driver of this malignant phenotype. Furthermore, hybrid cells showed greater sensitivity to the SLC7A5 inhibitor JPH203 compared to parental cells.

Conclusion

Fusion with MΦs confers enhanced malignancy to glioma cells, characterized by increased proliferation and invasion, which is promoted by the MΦ-derived gene SLC7A5. Targeting SLC7A5 represents a promising novel therapeutic strategy for glioma.