Downregulation of SNRPG induces cell cycle arrest and sensitizes human glioblastoma cells to temozolomide by targeting Myc through a p53-dependent signaling pathway.

Temozolomide (TMZ) is commonly used for glioblastoma multiforme (GBM) chemotherapy. However, drug resistance limits its therapeutic effect in GBM treatment. RNA-binding proteins (RBPs) have vital roles in posttranscriptional events. While disturbance of RBP-RNA network activity is potentially associated with cancer development, the precise mechanisms are not fully known. The gene, encoding small nuclear ribonucleoprotein polypeptide G, was recently found to be related to cancer incidence, but its exact function has yet to be elucidated. knockdown was achieved via short hairpin RNAs. Gene expression profiling and Western blot analyses were used to identify potential glioma cell growth signaling pathways affected by . Xenograft tumors were examined to determine the carcinogenic effects of on glioma tissues. The -mediated inhibitory effect on glioma cells might be due to the targeted prevention of Myc and p53. In addition, the effects of loss on p53 levels and cell cycle progression were found to be Myc-dependent. Furthermore, was increased in TMZ-resistant GBM cells, and downregulation of potentially sensitized resistant cells to TMZ, suggesting that deficiency decreases the chemoresistance of GBM cells to TMZ via the p53 signaling pathway. Our data confirmed that suppression sensitizes GBM cells to TMZ by targeting Myc via the p53 signaling cascade. These results indicated that is a probable molecular target of GBM and suggested that suppressing in resistant GBM cells might be a substantially beneficial method for overcoming essential drug resistance.