胶质母细胞瘤（GBM）被归类为四级胶质瘤。遗憾的是，目前没有治愈GBM的方法。Poly(rC)-binding蛋白1（PCBP1）是一种细胞质铁载体，具有多种功能。PCBP1也被认为在自噬中发挥调节作用，但PCBP1在铁依赖性细胞死亡通路——铁凋亡中——在GBM细胞中的作用仍未被揭示。在这里，我们研究了硼砂（一种硼化合物）对由PCBP1和自噬介导的铁凋亡信号通路的影响。该研究分析了在U87-MG和HMC3细胞上研究硼砂作用的细胞存活率、增殖和细胞周期。确定硼砂的细胞毒浓度后，进行了形态学分析以及对PCBP1、Beclin1、丙二醛（MDA）、谷胱甘肽（GSH）、谷胱甘肽过氧化物酶4（GPx4）和长链脂肪酰辅酶A合成酶家族成员4（ACSL4）水平的测量。最后，确定了PCBP1、Beclin1、GPx4和ACSL4的表达水平，以及caspase-3/7活性。我们发现，硼砂浓度和时间依赖地降低了U87-MG细胞的存活率。此外，硼砂改变了细胞增殖，显著降低了U87-MG细胞的S期，并通过对正常细胞（HMC3）产生相反的效果来展示其选择性。根据DAPI染色，硼砂导致U87-MG细胞的核缺陷。结果显示，在U87-MG细胞中，硼砂导致PCBP1、GSH和GPx4的降低，Beclin1、MDA和ACSL4的增加。此外，硼砂通过激活U87-MG细胞中的caspase 3/7触发细胞凋亡。我们的研究表明，硼砂通过调节PCBP1/Beclin1/GPx4/ACSL4信号通路对GBM有潜在的抗癌治疗作用。©2023 Wiley Periodicals LLC.

Glioblastoma (GBM) is classified as a stage-IV glioma. Unfortunately, there are currently no curative treatments for GBM. Poly(rC)-binding protein 1 (PCBP1) is a cytosolic iron chaperone with diverse functions. PCBP1 is also known to regulate autophagy, but the role of PCBP1 in ferroptosis, iron-dependent cell death pathway, remains unrevealed in GBM cells. Here, we investigated the effects of borax, a boron compound, on the ferroptosis signaling pathway mediated by PCBP1 and autophagy. The study analyzed cell viability, proliferation, and cell cycle on U87-MG and HMC3 cells to investigate the effects of borax. After determining the cytotoxic concentrations of borax, morphological analyzes and measurement of PCBP1, Beclin1, malondialdehyde (MDA), glutathione (GSH), glutathione peroxidase 4 (GPx4) and acyl-CoA synthetase long chain family member 4 (ACSL4) levels were performed. Finally, expression levels of PCBP1, Beclin1, GPx4 and ACSL4, and caspase-3/7 activity were determined. We found that borax reduced U87-MG cell viability in a concentration- and time-dependent manner. Additionally, borax altered cell proliferation and remarkably reduced S phase in the U87-MG cells and exhibited selectivity by having an opposite effect on normal cells (HMC3). According to DAPI staining, borax caused nuclear deficits in U87-MG cells. The result showed that borax in U87-MG cells induced reduction of the PCBP1, GSH, and GPx4 and enhancement of Beclin1, MDA, and ACSL4. Furthermore, borax triggered apoptosis by activating caspase 3/7 in U87-MG cells. Our study indicated that the borax has potential as an anticancer treatment for GBM via regulating PCBP1/Beclin1/GPx4/ACSL4 signaling pathways.© 2023 Wiley Periodicals LLC.