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<p>Low-density lipoprotein receptor-related protein 5 (LRP5), a co-receptor of frizzled (FZD) in the WNT/β-catenin signaling pathway, recognizes Wnt ligands. This study aimed to assess the anti-cancer effects of silencing <i>LRP5</i> on glioblastoma (GBM) and brain cancer stem cells (BCSCs). Additionally, the effect of temozolomide (TMZ) was also examined in these cells with suppressed <i>LRP5</i> expression. LRP5 expression was silenced in U87MG, T98G, and BCSC cells using siRNA. Protein expression levels were determined by Western blotting. Cell viability after <i>LRP5</i> silencing and/or TMZ treatment was evaluated using the CVDK-8 assay. Flow cytometry was used to examine apoptosis and cell cycle progression. Clonogenic, cell invasion, and wound-healing assays were used to assess colony formation, invasion, and migration, respectively. siRNA-mediated silencing reduced protein expression of LRP5 and Wnt/β-catenin target genes in GBM and BCSC cells. Furthermore, suppression of <i>LRP5</i> reduced cell viability, and its combination with TMZ enhanced anti-proliferative effects. Silencing <i>LRP5</i> and/or TMZ treatment caused cell cycle arrest and significantly diminished the aggressive characteristics of GBM and BCSC cells. These findings suggest that LRP5 may serve as a potential therapeutic target for treating GBM. Targeting LRP5 may enhance the effectiveness of the chemotherapy agent TMZ in GBM.</p>

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In vitro assessment of siRNA-mediated LRP5 silencing and temozolomide treatment in glioblastoma and brain cancer stem cells

  • 期刊论文

  • 发表日期：

    2026年1月31日

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  • Aslihan Kucuk,
  • Hasan Onur Caglar,
  • Omer Faruk Karatas,
  • Cigir Biray Avci,
  • Cumhur Gunduz

摘要

Low-density lipoprotein receptor-related protein 5 (LRP5), a co-receptor of frizzled (FZD) in the WNT/β-catenin signaling pathway, recognizes Wnt ligands. This study aimed to assess the anti-cancer effects of silencing LRP5 on glioblastoma (GBM) and brain cancer stem cells (BCSCs). Additionally, the effect of temozolomide (TMZ) was also examined in these cells with suppressed LRP5 expression. LRP5 expression was silenced in U87MG, T98G, and BCSC cells using siRNA. Protein expression levels were determined by Western blotting. Cell viability after LRP5 silencing and/or TMZ treatment was evaluated using the CVDK-8 assay. Flow cytometry was used to examine apoptosis and cell cycle progression. Clonogenic, cell invasion, and wound-healing assays were used to assess colony formation, invasion, and migration, respectively. siRNA-mediated silencing reduced protein expression of LRP5 and Wnt/β-catenin target genes in GBM and BCSC cells. Furthermore, suppression of LRP5 reduced cell viability, and its combination with TMZ enhanced anti-proliferative effects. Silencing LRP5 and/or TMZ treatment caused cell cycle arrest and significantly diminished the aggressive characteristics of GBM and BCSC cells. These findings suggest that LRP5 may serve as a potential therapeutic target for treating GBM. Targeting LRP5 may enhance the effectiveness of the chemotherapy agent TMZ in GBM.