STAC1 is required for glioblastoma cell invasion and survival

Glioblastoma Multiforme (GBM) is a highly malignant brain tumor with poor prognosis. Understanding the molecular mechanisms driving GBM tumorigenesis is crucial for developing effective therapeutic strategies. This study investigates the role of STAC1, a gene belonging to the SH3 and cysteine-rich domain family, in glioblastoma cell invasion and survival. Computational analyses of patient samples reveal that STAC1 expression is elevated in GBM tissues, and higher STAC1 expression is associated with lower overall survival rates. Consistently, we find that overexpression of STAC1 in glioblastoma cells enhances invasion, while knockdown of STAC1 reduces invasion and the expression of genes associated with epithelial-to-mesenchymal transition (EMT). STAC1 depletion also induces apoptosis in glioblastoma cells. Furthermore, we show that STAC1 regulates AKT and calcium channel signaling in glioblastoma cells. Collectively, our study provides valuable insights into the pathogenic roles of STAC1 in GBM and highlights its potential as a promising target for the treatment of high-grade glioblastoma.& COPY; 2023 Elsevier Inc. All rights reserved.

Automated summary

This study investigates the role of the gene STAC1 in glioblastoma cell invasion and survival. It is found that STAC1 overexpression promotes invasion and inhibits apoptosis, while knockdown of STAC1 has the opposite effect. The study also reveals that STAC1 regulates AKT and calcium channel signaling in glioblastoma cells. These findings provide valuable insights into the pathogenic roles of STAC1 in high-grade glioblastoma and highlight its potential as a promising therapeutic target.