Epigenetic modifications in chronic myeloid leukemia cells through ruxolitinib treatment
Makaleler > Tam Makale · 2018
Yazarlar: Çığır BİRAY AVCI, BAKİYE GÖKER BAĞCA, Aslı TETİK VARDARLI, Güray SAYDAM, Cumhur GÜNDÜZ
Journal of Cellular Biochemistry, SCI Expanded İndekslerine Giren Dergi, Uluslararası, Wos, 2018, cilt 120, ss 4555-4563
DOI: 10.1002/jcb.27744
Özet
Abstract Chronic myeloid leukemia is a clonal malignancy of hematopoietic stem cell that is characterized by the occurrence of t(9;22)(q34;q11.2) translocation, named Philadelphia chromosome. Ruxolitinib is a powerful Janus tyrosine kinase 1 and 2 inhibitor that is used for myelofibrosis treatment. DNA‐histone connection mediates a wide range of genes that code methylation, demethylation, acetylation, deacetylation, ubiquitination, and phosphorylation enzymes. Epigenetic modifications regulate chromatin compactness, which plays pivotal roles in critical biological processes including the transcriptional activity and cell proliferation as well as various pathological mechanisms, including CML. This study is aimed to determine the alterations of the expression levels of epigenetic modification–related genes after ruxolitinib treatment. Total RNA was isolated from K‐562 cells treated with the IC50 value of ruxolitinib and untreated K‐562 control cells. A reverse transcription procedure was performed for complementary DNA synthesis, and gene expressions were detected by real‐time polymerase chain reaction compared with the untreated cells. Ruxolitinib treatment caused a significant alteration in the expression levels of epigenetic regulation‐related genes in K‐562 cells. Our novel results suggested that ruxolitinib has inhibitor effects on epigenetic modification–regulator genes.