Abstract
Cluster of differentiation (CD) 73, which is encoded by the NT5E gene, regulates production of immunosuppressive adenosine and is an emerging checkpoint in cancer immunotherapy. Despite the significance of CD73 in immuno-oncology, the roles of the NT5E gene methylation in breast cancer have not been well-defined yet. Therefore, we aimed to investigate the prognostic significance of the NT5E gene methylation in breast cancer. The DNA methylation status of the NT5E gene was analyzed using pyrosequencing in breast cancer tissues. In addition, the levels of inflammatory markers and lymphocyte infiltration were evaluated. The mean methylation level of the NT5E gene was significantly higher in breast cancer than in normal breast tissues. In the analysis of relevance with clinicopathologic characteristics, the mean methylation levels of the NT5E gene were significantly higher in patients with large tumor size, high histologic grade, negative estrogen receptor expression, negative Bcl-2 expression, and premenopausal women. There was no difference in disease-free survival according to the methylation status of the NT5E gene. We found that the NT5E gene methylation was related to breast cancer development and associated with poor prognostic factors in breast cancer. Our results suggest that the NT5E gene methylation has potential as an epigenetic biomarker in breast cancer.
Highlights
Cluster of differentiation (CD) 73 is a glycosylphosphatidylinositol-anchored cell surface protein known as an ecto-50 -nucleotidase (NT5E), which is encoded by the NT5E gene [1]
The methylation status of the NT5E gene was significantly different between breast cancer tissue
We report that the NT5E gene methylation is related to breast cancer development and is associated with poor prognostic factors in breast cancer
Summary
Cluster of differentiation (CD) 73 is a glycosylphosphatidylinositol-anchored cell surface protein known as an ecto-50 -nucleotidase (NT5E), which is encoded by the NT5E gene [1]. CD73 plays a critical role in the catabolism of extracellular adenosine monophosphate (AMP) into adenosine, which suppresses antitumor immunity in the tumor microenvironment [3]. In this context, CD73 and downstream adenosine receptors have emerged as novel therapeutic targets in cancer immunotherapy [3,4]. The impacts of the CD73-adenosinergic pathway and mechanism of antitumor immunity have increasingly been recognized [5,6,7]. Targeting the CD73-adenosinergic pathway in preclinical studies showed favorable antitumor effects [8] and early-phase clinical trials showed promising results [7]
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