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.

This study aims to clarify the mechanistic actions of microRNA-873-5p (miR-873-5p) on glioblastoma (GBM) progression. The most differentially expressed miRNAs were retrieved from the GEO database. It was established that miR-873-5p was downregulated in GBM tissues and cells. Based on in silico prediction and experimental data, HMOX1 was demonstrated to be a target gene of miR-873-5p. Further, miR-873-5p was then ectopically expressed in GBM cells to examine its effect on the malignant behaviors of GBM cells. Overexpression of miR-873-5p inhibited GBM cell proliferation and invasion by targeting HMOX1. HMOX1 promoted SPOP expression by increasing HIF1α expression, thus stimulating GBM cell malignant phenotypes. miR-873-5p suppressed the malignant phenotypes of GBM cells and tumorigenesis in vitro and in vivo by inhibiting the HMOX1/HIF1α/SPOP signaling axis. This study uncovers a novel miR-873-5p/HMOX1/HIF1α/SPOP axis in GBM, providing new insights into GBM progression and therapeutic targets for GBM treatment.