KOENZİM Q0 İNSAN KRONİK MYELOİD LÖSEMİ K562 HÜCRELERİNİN PROLİFERASYONUNU ENGELLER VE MAPK VE AKT SİNYAL YOLAKLARINI MODÜLE EDER
-
Published:2023-06-12
Issue:3
Volume:47
Page:5-5
-
ISSN:1015-3918
-
Container-title:Ankara Universitesi Eczacilik Fakultesi Dergisi
-
language:en
-
Short-container-title:Ankara Ecz. Fak. Derg.
Author:
KAYA SEZGİNER Ecem1ORCID, YAPRAK Ali1ORCID, KARABAY Arzu Zeynep1ORCID
Affiliation:
1. ANKARA ÜNİVERSİTESİ, ECZACILIK FAKÜLTESİ, TEMEL ECZACILIK BİLİMLERİ BÖLÜMÜ, BİYOKİMYA ANABİLİM DALI
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.
Publisher
Ankara Universitesi Eczacilik Fakultesi Dergisi
Subject
Pharmaceutical Science,Pharmacology
Reference60 articles.
1. 1. Faderl, S., Talpaz, M., Estrov, Z., O'Brien, S., Kurzrock, R., Kantarjian, H.M. (1999). The biology of chronic myeloid leukemia. New England Journal of Medicine, 341(3), 164-172. [CrossRef] 2. 2. Chereda, B., Melo, J.V. (2015). Natural course and biology of CML. Annals of Hematology, 94(Suppl 2), S107-121. [CrossRef] 3. 3. Druker, B.J., Talpaz, M., Resta, D.J., Peng, B., Buchdunger, E., Ford, J.M., Lydon, N.B., Kantarjian, H., Capdeville, R., Ohno-Jones, S., Sawyers, C.L. (2001). Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia. New England Journal of Medicine, 344(14), 1031-1037. [CrossRef] 4. 4. Kantarjian, H.M., Talpaz, M. (2001). Imatinib mesylate: Clinical results in Philadelphia chromosome-positive leukemias. Seminars in Oncology, 28(5 Suppl 17), 9-18. [CrossRef] 5. 5. Mohamed, A.N., Pemberton, P., Zonder, J., Schiffer, C.A. (2003). The effect of imatinib mesylate on patients with Philadelphia chromosome-positive chronic myeloid leukemia with secondary chromosomal aberrations. Clinical Cancer Research, 9(4), 1333-1337.
|
|