The effect of radiation-induced genotoxic stress on the expression of satellite II and satellite III repeats in breast and colon cancer cells
INTERNATIONAL JOURNAL OF RADIATION RESEARCH, sa.1, 2024 (SCI-Expanded)
- Yayın Türü: Makale / Tam Makale
- Basım Tarihi: 2024
- Doi Numarası: 10.61186/ijrr.22.1.91
- Dergi Adı: INTERNATIONAL JOURNAL OF RADIATION RESEARCH
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED)
- Açık Arşiv Koleksiyonu: AVESİS Açık Erişim Koleksiyonu
- İstanbul Üniversitesi Adresli: Evet
Özet
Background: Pericentric human satellite II (HSATII) and III (HSATIII) have been shown to be associated with stress response. Expression status of these satellite repeats has not yet been investigated under radiation-induced genotoxic stress. We evaluated the HSATII and HSATIII expression changes under genotoxic stress in cancer cells. Materials and Methods: Cell line MCF-7 and cell line HCT-15 were irradiated with 2 and 5 Gy of ionizing radiation, and cell death rates, as a consequence of genotoxic stress, were determined by flow cytometry. The expression of HSATII and HSATIII expressions was assessed by RT-qPCR. Results: Radiation exposure induced a considerable level of cell death in a dose-dependent manner in both cell types. Compared to untreated cells, HSATII expression declined in MCF-7 cells which were exposed to 2 and 5 Gy radiation, respectively. In HCT-15 cells, the effect of radiation on the HSATII expression was not unified; only higher radiation dose led to a decrease of HSATII expression while 2 Gy increased HSATII expression. The effect of radiation on the HSATIII repeat expression was more pronounced in HCT-15 cells: in MCF-7 cells, HSATIII expression was decreased by 2- and 5-Gy, respectively (p=0.01). In the HCT-15 cells, the rates of HSATIII down-regulation were 3-fold and 2.8 fold by 2- and 5 Gy (p=0.0002 and p=0.02, respectively). Conclusion: Our findings reveal that genotoxic stress induced by ionizing radiation is associated with a decrease in the expression of pericentric satellites and the expression status of HSATII in these conditions may be dose- and/or cellular context-specific.