- Ankara Üniversitesi Eczacılık Fakültesi Dergisi
- Cilt: 47 Sayı: 3
- COENZYME Q0 INHIBITS CELL PROLIFERATION AND MODULATES MAPK AND AKT SIGNALLING PATHWAYS IN HUMAN CHRO...
COENZYME Q0 INHIBITS CELL PROLIFERATION AND MODULATES MAPK AND AKT SIGNALLING PATHWAYS IN HUMAN CHRONIC MYELOID LEUKEMIA K562 CELLS
Authors : Ecem Kaya Sezginer, Ali Yaprak, Arzu Zeynep Karabay
Pages : 761-769
Doi:10.33483/jfpau.1286359
View : 47 | Download : 70
Publication Date : 2023-09-20
Article Type : Research
Abstract :Objective: This study evaluated the antiproliferative and pro-apoptotic effects of coenzyme Q0 (CoQ0) in human chronic myeloid leukemia K562 cell line. Material and Method: The cytotoxic effect of CoQ0 on human chronic myeloid leukemia cell line, K562 was determined by MTT test. The activity of caspase-3, expression of proteins involved in apoptosis, MAPK and AKT signaling pathways were determined with enzymatic assay and western blot analysis, respectively. Result and Discussion: Results showed that CoQ0 inhibited cell viability of K562 cells at 5 μM and higher concentrations and Bax protein expression was significantly decreased at 12.5 μM concentration of CoQ0. However, CoQ0 did not significantly affect caspase 3 activity and Bcl-2 protein expression. p-c-Raf (Ser259) protein expression was significantly decreased at 12.5 μM of CoQ0. Treatment with 10 μM of CoQ0 induced significantly phosphorylation of p38 MAPK and 12.5 μM CoQ0 caused a nonsignificant decrease in p-ERK1/2 protein expression in K562 cell line. Interestingly, in K562 cells, phosphorylation of Akt (Ser473) was diminished at 12.5 μM of CoQ0, with no change observed in p-Akt (Thr308) protein expression among groups. In conclusion, CoQ0 inhibited cell proliferation and suppressed phosphorylation of c-Raf (Ser259), Akt (Ser473), but not ERK1/2 in K562 cells. There is still a need for new insights into the anticancer mechanisms of CoQ0 and develop treatment strategies for chronic myeloid leukemia.Keywords : Koenzim Q0, kronik miyeloid lösemi, K562