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. Thegene, 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 ofon glioma tissues.The-mediated inhibitory effect on glioma cells might be due to the targeted prevention of Myc and p53. In addition, the effects ofloss on p53 levels and cell cycle progression were found to be Myc-dependent. Furthermore,was increased in TMZ-resistant GBM cells, and downregulation ofpotentially sensitized resistant cells to TMZ, suggesting thatdeficiency decreases the chemoresistance of GBM cells to TMZ via the p53 signaling pathway. Our data confirmed thatsuppression sensitizes GBM cells to TMZ by targeting Myc via the p53 signaling cascade.These results indicated thatis a probable molecular target of GBM and suggested that suppressingin resistant GBM cells might be a substantially beneficial method for overcoming essential drug resistance. Objective: Methods: Results: Conclusions: SNRPG SNRPG SNRPG SNRPG SNRPG SNRPG SNRPG SNRPG SNRPG SNRPG SNRPG SNRPG
