Kenalog modified by ionizing radiation induces intrinsic apoptosis mediated by elevated levels of reactive oxygen species in melanoma cancer

Kenalog is a synthetic glucocorticoid drug used to treat various cancers including ocular and choroidal melanoma. However, the drug achieves rarely sustainable results for patients. To overcome this difficulty, the structure of Kenalog was altered by ionizing radiation (IR) to develop a more effecti...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Oncology reports 2019-03, Vol.41 (3), p.1837-1850
Hauptverfasser: Kawala, Remigius Ambrose, Ramadhani, Fatuma Jumapili, Choi, Hyo Jin, Lee, Eun-Hee, Park, Chul-Hong, Chung, Byung Yeoup, Bai, Hyoung-Woo
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Kenalog is a synthetic glucocorticoid drug used to treat various cancers including ocular and choroidal melanoma. However, the drug achieves rarely sustainable results for patients. To overcome this difficulty, the structure of Kenalog was altered by ionizing radiation (IR) to develop a more effective anticancer agent for treatment of various skin cancers. The anticancer effect of modified Kenalog (Kenalog‑IR) was assessed in melanoma cancer cells in vitro. The assessment of mitochondrial functions by MTT assay revealed significant inhibition of melanoma cancer cell viability by Kenalog‑IR compared to Kenalog. Moreover, Kenalog‑IR‑induced apoptotic cell death was associated with the intrinsic mitochondrial pathway by triggering the release of intrinsic apoptosis molecules through activation of caspase‑related molecules in concentration and time‑dependent manners. Furthermore, it was observed that Kenalog‑IR‑induced apoptosis was associated with the generation of reactive oxygen species (ROS) with increased G2/M cell cycle arrest. Collectively, Kenalog‑IR may be a potential suppressor of skin‑related cancer in particular melanoma cancer.
ISSN:1021-335X
1791-2431
DOI:10.3892/or.2018.6940