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<p>Human discs large-associated protein 5 (DLGAP5), also known as DLG7, is a crucial protein associated with the mitotic spindle and is increased in different types of tumours. Nevertheless, its role in glioblastoma (GBM) remain poorly understood. Therefore, the purpose of this work was to examine the mechanisms and biological functions of DLGAP5 in GBM. Furthermore, we investigated how DLGAP5 affected the polarisation of tumor-associated macrophages (TAMs). We assessed the growth, migration, and invasion of GBM cells using a cell counting kit (CCK8), 5-Ethynyl-2’-deoxyuridine (EdU) incorporation, wound healing, and Transwell assays. The expression levels of TAM-associated differentiation markers CD68, CD206, and CD11b were examined by flow cytometry. The effects of tumour cell-derived DLGAP5 on THP-1 macrophage polarisation were investigated using a coculture paradigm including GBM cells and differentiated THP-1 cells. The effect of DLGAP5 on carcinogenesis in vivo was also investigated using a xenograft nude mice model. DLGAP5 was found to be upregulated in both GBM tissues and cell lines. The knockdown of DLGAP5 inhibited GBM cell proliferation, migration, and invasion, as well as M2 polarization of TAMs. In an in vivo model, suppression of DLGAP5 led to decreased tumor growth. Our findings indicate that DLGAP5 significantly promotes the malignant phenotype of GBM. These findings have potential implications for the future diagnosis and therapy of GBM.</p>

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DLGAP5 facilitates glioblastoma growth and tumor-associated macrophage M2 polarization

  • 期刊论文

  • 发表日期：

    2025年9月13日

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  • Fujun Chen,
  • Yong Luo,
  • Fenghong Lv,
  • Hongmin Li

摘要

Human discs large-associated protein 5 (DLGAP5), also known as DLG7, is a crucial protein associated with the mitotic spindle and is increased in different types of tumours. Nevertheless, its role in glioblastoma (GBM) remain poorly understood. Therefore, the purpose of this work was to examine the mechanisms and biological functions of DLGAP5 in GBM. Furthermore, we investigated how DLGAP5 affected the polarisation of tumor-associated macrophages (TAMs). We assessed the growth, migration, and invasion of GBM cells using a cell counting kit (CCK8), 5-Ethynyl-2’-deoxyuridine (EdU) incorporation, wound healing, and Transwell assays. The expression levels of TAM-associated differentiation markers CD68, CD206, and CD11b were examined by flow cytometry. The effects of tumour cell-derived DLGAP5 on THP-1 macrophage polarisation were investigated using a coculture paradigm including GBM cells and differentiated THP-1 cells. The effect of DLGAP5 on carcinogenesis in vivo was also investigated using a xenograft nude mice model. DLGAP5 was found to be upregulated in both GBM tissues and cell lines. The knockdown of DLGAP5 inhibited GBM cell proliferation, migration, and invasion, as well as M2 polarization of TAMs. In an in vivo model, suppression of DLGAP5 led to decreased tumor growth. Our findings indicate that DLGAP5 significantly promotes the malignant phenotype of GBM. These findings have potential implications for the future diagnosis and therapy of GBM.