Akademik Veri Yönetim Sistemi
MEANDROS MEDICAL AND DENTAL JOURNAL, sa.4, ss.351-364, 2024 (ESCI)
Objective: Cell-free DNAs (cf-DNAs) are released into the bloodstream through cell apoptosis, necrosis, or active secretion, often originating from cancer cells. These cf-DNAs have been associated with cancer development and metastasis, although their precise role remains under debate. DNase I, an enzyme that degrades extracellular DNA, has shown potential to impact cf-DNAs and influence cancer progression. This study investigates the effects of ovarian cancer cells on the proliferation and viability of non-tumorigenic breast cells, with a focus on DNase I's role. Materials and Methods: Human ovarian cancer cells (OVCAR-3) and normal human breast cells (MCF10A) were cultured under standard conditions (37 degrees C, 5% CO2). Co-culture experiments were conducted by incubating cells separately in plates and inserts, with or without DNase I, for 72 hours. Cell viability was assessed using the trypan blue exclusion test, while proliferation and adhesion were measured with an XTT assay. Results: DNase I significantly reduced OVCAR-3 proliferation (p<0.001) and adhesion (p<0.01) without affecting MCF-10A cells. DNase I also decreased OVCAR-3 cell viability but did not significantly impact MCF-10A viability. Genetic analysis identified p53 exon 7 mutations and methylation of APC1A, APC1B, and RASSF1A genes in OVCAR-3 cells, which were unaffected by DNase I. No mutations or methylation were detected in MCF-10A cells. Conclusion: The results suggest that the impact of DNase I on the proliferation and viability of cancer cells is significant and warrants further investigation. The potential effects of prolonged exposure between different cell types could yield even more compelling findings.