Abstract
Many studies have reported an increase in the level of circulating cell-free DNA (cfDNA) in the blood of patients with cancer. cfDNA mainly comes from tumor cells and, therefore, carries features of its genomic profile. Moreover, tumor-derived cfDNA can act like oncoviruses, entering the cells of vulnerable organs, transforming them and forming metastatic nodes. Another source of cfDNA is immune cells, including neutrophils that generate neutrophil extracellular traps (NETs). Despite the potential eliminative effect of NETs on tumors, in some cases, their excessive generation provokes tumor growth as well as invasion. Considering both possible pathological contributions of cfDNA, as an agent of oncotransformation and the main component of NETs, the study of deoxyribonucleases (DNases) as anticancer and antimetastatic agents is important and promising. This review considers the pathological role of cfDNA in cancer development and the role of DNases as agents to prevent and/or prohibit tumor progression and the development of metastases.
Highlights
The presence of cell-free DNA in blood plasma was first described by Mandel and Métais in 1948 [1]
This review considers the pathological role of cell-free DNA (cfDNA) in cancer development and the role of DNases as agents to prevent and/or prohibit tumor progression and the development of metastases
We focus on the role of tumor-derived cfDNA in tumor progression, the pro-tumor and anti-tumor effects of neutrophil extracellular traps (NETs) and the involvement of DNases in the regulation of DNA-mediated metastasis and tumor dissemination
Summary
The presence of cell-free DNA (cfDNA) in blood plasma was first described by Mandel and Métais in 1948 [1]. An increased level of microsatellite fragments, tandem repeats and mobile genetic elements (MGE) is usually detected in the blood-derived cfDNA pool at the early stages of the development of both experimental tumors and various tumors in patients [6,7,8,9] These sequences are considered promising prognostic and diagnostic markers in oncology. According to the genometastatic hypothesis, ‘metastases can occur by transfection of vulnerable cells located in the target organs with tumor-specific DNA from cells of the primary tumor circulating in the blood plasma’ [10] This hypothesis has been accepted by other authors as a model that could explain the inconsistencies in experimental data regarding metastasis [11]. We focus on the role of tumor-derived cfDNA in tumor progression, the pro-tumor and anti-tumor effects of NETs and the involvement of DNases in the regulation of DNA-mediated metastasis and tumor dissemination
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