Glioma is the most common primary malignancy in the brain, and vasculogenic mimicry (VM) is one of the blood supply methods. Here we investigated the possibility that lncRNAs regulate the stability of transcription factors through the SMD pathway, which affects proliferation, migration, invasion, and the ability to form VMs in glioma. Expression of PABPC5, HCG15, and ZNF331 was detected by real-time qPCR or western blot in glioma. Cell Counting Kit-8, Transwell assays, and in vitro VM tube formation were used to investigate PABPC5, HCG15, and ZNF331 function in cell proliferation, migration, invasion, and VM, respectively. ChIP assays were used to ascertain the interaction betweenZNF331 and LAMC2 or PABPC5. PABPC5 and HCG15 were highly expressed in glioma cells. ZNF331 was lowly expressed. PABPC5 bound HCG15 to increase its stability. Knockdown HCG15 reduced the degradation of ZNF331 mRNA by the SMD pathway. ZNF331 inhibited transcription through binding to the promoter region of LAMC2 and PABPC5 and inhibited the ability to form VMs in glioma cells. The PABPC5/HCG15/ZNF331 feedback loop plays an important role in regulating VM formation in glioma and provides new targets for glioma treatment.

脑胶质瘤是脑中最常见的原发性恶性肿瘤，而血管生成模拟物（VM）是一种血液供应方法。在这里，我们调查了lncRNA通过SMD途径调节转录因子稳定性的可能性，这会影响神经胶质瘤中的增殖，迁移，侵袭和形成VM的能力。通过实时qPCR或western blot检测胶质瘤中PABPC5，HCG15和ZNF331的表达。使用Cell Counting Kit-8，Transwell分析和体外VM管形成研究PABPC5，HCG15和ZNF331分别在细胞增殖，迁移，侵袭和VM中起作用。用ChIP分析确定ZNF331与LAMC2或PABPC5之间的相互作用。PABPC5和HCG15在神经胶质瘤细胞中高表达。ZNF331表达不足。PABPC5势必HCG15以增加其稳定性。敲除HCG15由SMD途径减少ZNF331 mRNA的降解。ZNF331通过与LAMC2和PABPC5的启动子区结合来抑制转录，并抑制在神经胶质瘤细胞中形成VM的能力。的PABPC5 / HCG15 / ZNF331反馈回路在调节神经胶质瘤中VM形成中起重要作用，并为神经胶质瘤治疗提供了新的靶点。