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CD73 in glioblastoma: Where are we now and what are the future directions?
Nicolly Espindola Gelsleichter1, Juliana Hofstätter Azambuja2, Dominique Santos Rubenich1
1Programa de Pós-Graduação em Biociências, Universidade Federal de Ciências da Saúde de Porto Alegre, (UFCSPA), Porto Alegre, RS, Brazil.
Abstract:
Glioblastoma (GB) is the most aggressive type of brain tumor with heterogeneity, strong invasive ability, and high resistance to therapy due to immunosuppressive mechanisms. CD73 is an overexpressed enzyme in GB that acts via two main mechanisms: (1) CD73 acts as an adhesion protein independent of the enzymatic activity or (2) via the catalyses of AMP to adenosine (ADO) generating a strong modulatory molecule that induces alterations in the tumor cells and in the tumor microenvironment cells (TME). Taken together, CD73 is receiving attention during the last years and studies demonstrated its dual potential benefit as a target to GB therapy. Here, we review the roles of CD73 and P1 receptors (ADO receptors) in GB, the impact of CD73 in the immune interactions between tumor and other immune cells, the proposed therapeutic strategies based on CD73 regulation, and discuss the gap in knowledge and further directions to bring this approach from preclinical to clinical use.
Insights
CD73, an enzyme overexpressed in glioblastoma (GB), presents dual therapeutic potential. Targeting CD73 and adenosine receptors may overcome treatment resistance in this aggressive brain tumor.
Area of Science:
- Oncology
- Immunology
- Biochemistry
Background:
- Glioblastoma (GB) is an aggressive brain tumor characterized by heterogeneity, invasiveness, and therapeutic resistance, often linked to immunosuppressive mechanisms.
- CD73 is frequently overexpressed in GB, playing a critical role through its enzymatic activity (AMP to adenosine conversion) and as an adhesion molecule.
- Adenosine, generated by CD73, significantly modulates tumor cells and the tumor microenvironment (TME), contributing to immune evasion.
Purpose of the Study:
- To review the multifaceted roles of CD73 and adenosine (ADO) receptors in glioblastoma.
- To elucidate the impact of CD73 on immune cell interactions within the tumor microenvironment.
- To discuss current and proposed therapeutic strategies targeting CD73 for glioblastoma treatment and identify future research directions.
Main Methods:
- Literature review of studies on CD73 and adenosine receptors in glioblastoma.
- Analysis of CD73's dual mechanisms: enzymatic activity and cell adhesion.
- Examination of CD73's influence on tumor-immune cell interactions and the TME.
- Synthesis of proposed therapeutic strategies targeting CD73 regulation.
Main Results:
- CD73 contributes to glioblastoma's aggressive phenotype and therapeutic resistance via adenosine production and adhesion properties.
- Adenosine signaling through P1 receptors impacts immune cell function, promoting an immunosuppressive TME.
- CD73's dual role offers potential therapeutic avenues, but clinical translation requires further investigation.
Conclusions:
- CD73 is a promising therapeutic target in glioblastoma due to its significant role in tumor progression and immune evasion.
- Understanding the interplay between CD73, adenosine, and immune cells is crucial for developing effective anti-GB therapies.
- Bridging the gap between preclinical findings and clinical application of CD73-targeted strategies is essential for improving patient outcomes.
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