Selenium potentiates the anticancer effect of cisplatin against oxidative stress and calcium ion signaling induced intracellular toxicity in MCF 7 breast cancer cells involvement of the TRPV1 channel
Yazarlar (5)
Esin Sakallı Çetin
Muğla Sıtkı Koçman Üniversitesi, Türkiye
Mustafa Nazıroğlu
Süleyman Demirel University, Faculty Of Medicine, Türkiye
Doç. Dr. Bilal ÇİĞ
Süleyman Demirel University, Faculty Of Medicine, Türkiye
İshak Suat Övey
Süleyman Demirel University, Faculty Of Medicine, Türkiye
Pınar Aslan Koşar
Süleyman Demirel University, Faculty Of Medicine, Türkiye
| Makale Türü | Özgün Makale (SSCI, AHCI, SCI, SCI-Exp dergilerinde yayınlanan tam makale) | ||
| Dergi Adı | Journal of Receptors and Signal Transduction | ||
| Dergi ISSN | 1079-9893 Wos Dergi Scopus Dergi | ||
| Dergi Tarandığı Indeksler | SCI | ||
| Makale Dili | İngilizce | Basım Tarihi | 02-2017 |
| Cilt / Sayı / Sayfa | 37 / 1 / 84–93 | DOI | 10.3109/10799893.2016.1160931 |
| Makale Linki | https://www.tandfonline.com/doi/full/10.3109/10799893.2016.1160931 | ||
| Özet |
| Background: In breast cancers, calcium signaling is a main cause of proliferation and apoptosis of breast cancer cells. Although previous studies have implicated the transient receptor potential vanilloid 1 (TRPV1) cation channel, the synergistic inhibition effects of selenium (Se) and cisplatin in cancer and the suppression of ongoing apoptosis have not yet been investigated in MCF-7 breast cancer cells. This study investigates the anticancer properties of Se through TRPV1 channel activity in MCF-7 breast cancer cell line cultures when given alone or in combination with cisplatin. Materials: The MCF-7 cells were divided into four groups: the control group, the Se-treated group (200nM), the cisplatin-treated group (40M) and the Se+cisplatin-treated group. Results: The intracellular free calcium ion concentration and current densities increased with TRPV1 channel activator capsaicin (0.01mM), but they decreased with the TRPV1 blocker capsazepine (0.1mM), Se, cisplatin, and Se+cisplatin incubations. However, mitochondrial membrane depolarization, apoptosis, and the caspase 3, and caspase 9 values increased in the Se-treated group and the cisplatin-treated group, although Western blot (procaspase 3 and 9) results and the cell viability levels decreased with the Se and Se+cisplatin treatments. Apoptosis and caspase-3 were further increased with the Se+cisplatin treatment. Intracellular reactive oxygen species production increased with the cisplatin treatment, but not with the Se treatment. Conclusion: This study's results report, for the first time, that at a cellular level, Se and cisplatin interact on the same intracellular toxic cascade, and the combination of these two drugs can result in a remarkable anticancer effect through modulation of the TRPV1. |
| Anahtar Kelimeler |
| Apoptosis | breast cancer | calcium signaling | cisplatin | oxidative stress | TRPV1 channel |
BM Sürdürülebilir Kalkınma Amaçları
| Atıf Sayıları | |
| WoS | 64 |
| SCOPUS | 67 |