Avaliação da expressão gênica das ectoenzimas CD39 e CD73 em tecidos humanos de Glioblastomas e Gliomas não Glioblastomas por qRT-PCR

Abstract

Glioblastoma (GBM) and gliomas are the most prevalent malignant tumors affecting the central nervous system. Their high degree of aggressiveness and invasiveness is closely associated with elevated extracellular adenosine levels, a well-established immunosuppressive mediator within the tumor microenvironment. Increased expression of the ectonucleotidases CD39 and CD73 plays a pivotal role in adenosine metabolism, contributing to tumor progression and immune evasion. This study aimed to characterize the patients included in the cohort and to evaluate the relative mRNA expression of CD39 and CD73 in brain tissue samples obtained from patients with GBM and gliomas. A quantitative, cross-sectional study was conducted involving 36 patients allocated into two groups: 16 patients with GBM and 20 patients with gliomas, all of whom underwent surgical tumor resection. Clinical and demographic data were obtained from medical records, and all participants provided written informed consent. Relative mRNA expression of CD39 and CD73 was quantified using quantitative real-time polymerase chain reaction (qRT-PCR). The results demonstrated that approximately 75% of patients with gliomas were younger than 50 years at the time of tumor resection, whereas 90% of patients with GBM were older than 50 years. Most gliomas were classified as World Health Organization (WHO) grade II tumors. Relative mRNA expression levels of both CD39 and CD73 were significantly higher in the GBM group compared with the glioma group (CD39: p < 0.0083; CD73: p < 0.0069). CD73 is recognized as a key regulator of tumor invasiveness, metastatic potential, and aggressiveness, as well as reduced overall survival, owing to its central role in extracellular adenosine production. Adenosine generation may result from the synergistic interaction between tumor-infiltrating T cells, which overexpress CD39, and tumor cells, which overexpress CD73. Further investigations employing complementary approaches, such as immunohistochemistry, are warranted to confirm CD73 overexpression at the protein level. Future studies should also explore the therapeutic silencing of these purinergic pathways to reduce extracellular adenosine production and promote tumor regression, particularly in GBM, given its poor prognosis and two-year survival rate of less than 10%.