Background

Glioblastoma (GBM) is the most common malignant tumor of the central nervous system [1]. It is characterized by invasive growth and easy recurrence [2]. Recently, despite continuous developments in treatment methods, such as surgery, radiotherapy, and chemotherapy have been reported, the median survival time of patients remains 12–15 months, and no substantial improvement has been achieved yet [29]. Changes in lncRNA expression and its mutation can promote the occurrence and metastasis of tumors [30]. lncRNA plays a key role in TME intracellular signal transduction [31]. GABPB1-AS1 is an lncRNA in the cytoplasm. Recently, many studies have pointed out that lncRNA is a poor prognosis marker of glioma [32], cervical cancer [33], breast cancer [34], and prostate cancer [35]. According to this study, significant differences in GABPB1-AS1 expression was found between tumor and normal tissues. Similarly, Li et al. [36] found high expression of GABPB1-AS1 in the glioma tissues, and in vitro and in vivo experiments have demonstrated that GABPB1-AS1 knockdown reduced the proliferation and invasiveness of glioma cells. According to our results, Hsa-miR-519c-5p can be regulated by GABPB1-AS1 specifically, thus regulating the transcriptional levels of CASP3 and TP63. On this basis, Hsa-miR-519c-5p can control ECM-related signaling pathways (e.g., ECM receptor interaction, adherens junction, and TGFβ signaling pathways) and immune-related signaling pathways (e.g., Toll-like receptor and NOD-like receptor signaling pathways). This demonstrated that ECM and immune inflammation reactions played the key role in occurrence, invasion and metastasis of GBM. The TGF-β in the tumor tissues can inhibit immune cells, decrease local inflammation, and promote the reconstruction of ECM [37]. ECM components and high expression levels on the corresponding cell surface receptors are closely related with the progression of GBM [38]. Toll-like receptors (TLRs) can recognize non-self-molecules and activate the inflammation process. TLR expression had been observed in various samples, such as GBM cases and GBM cell lines, indicating that TLR plays an important role in tumor invasion and metastasis [39]. Therefore, we speculated that the mechanism by which GABPB1-AS1 regulates the transcriptional levels of CASP3 and TP63 and relevant signaling pathways through Hsa-miR-519c-5p might play a crucial role in the occurrence and development of GBM.

Conclusions

In conclusion, pyroptosis and TME-related independent prognostic markers were screened, and a prognosis risk score formula was established for the first time on the basis of prognosis PRGs. TME immunocyte infiltration characterization and immune response were assessed with ssGSEA, CIBERSORT algorithm, TIMER, and TISIDB database. A ceRNA network was then constructed. This study not only laid the foundation for the further exploration of pyroptosis and TME for the improvement of GBM prognosis but also provided novel insights for clinical immunotherapy and development of novel immunotherapeutic drugs. Deep experimental and clinical studies are still needed to elucidate the molecular mechanism of GBM and clinical applications of biomarkers and immunotherapy.