AI Article Synopsis
- Epithelial-mesenchymal transition (EMT) plays a crucial role in cancer progression, invasion, and resistance to therapy, making it an important target for cancer research.
- The CD73 enzyme has been linked to EMT, as it produces adenosine, which influences cell adhesion and migration, as well as having immunosuppressive effects.
- An analysis of RNA sequencing data identified a strong correlation between EMT scores and the expression of CD73 and CD39 in various cancers, especially prostate adenocarcinoma, indicating that the interplay between EMT and the adenosine signaling pathway varies by tumor context and could lead to new treatment approaches.
Article Abstract
Epithelial-mesenchymal transition (EMT) is a key mechanism related to tumor progression, invasion, metastasis, resistance to therapy and poor prognosis in several types of cancer. However, targeting EMT or partial-EMT, as well as the molecules involved in this process, has remained a challenge. Recently, the CD73 enzyme, which hydrolyzes AMP to produce adenosine (ADO), has been linked to the EMT process. This relationship is not only due to the production of the immunosuppressant ADO but also to its role as a receptor for extracellular matrix proteins, being involved in cell adhesion and migration. This article reviews the crosstalk between the adenosinergic pathway and the EMT program and the impact of this interrelation on cancer development and progression. An in silico analysis of RNAseq datasets showed that several tumor types have a significant correlation between an EMT score and NT5E (CD73) and ENTPD1 (CD39) expressions, with the strongest correlations being in prostate adenocarcinoma. Furthermore, it is evident that the cooperation between EMT and the adenosinergic pathway in tumor progression is context and tumor-dependent. The increased knowledge about this topic will help broaden the view to explore new treatments and therapies for different types of cancer.
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| http://dx.doi.org/10.1016/j.semcancer.2022.06.012 | DOI Listing |
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