MOLECULAR INVESTIGATION OF LONG NON CODING RNA EXPRESSION IN THYROISINE KINASE INHIBITOR IMATINIB SENSITIVE AND RESISTANT CHRONIC MYELOID LEUKEMIA CELL MODELS
Project no. 34 · Status: Kapanmış · 2016
Summary
Chronic myeloid leukemia (CML) is a hematological disease resulting from generation of BCR/ABL oncogene by philadelphia chromosome. Long non-coding RNAs (lncRNAs) are non-coding RNAs that are > 200nt, and many have been found to be involved in many epigenetic mechanisms such as chromatin modification, genomic imprinting, and regulation of gene expression. Imatinib, a tyrosine kinase inhibitor(TKI) that targets BCR-ABL and greatly improves prognosis for CML. However, the emergence of TKI resistance, largely due to mutation of the ABL kinase domain is a major problem. In this study we aimed to evaluate the cytotoxic effect of imatinib in CML cells by altering long non coding RNAs expression levels and gene expression of lnc RNAs targets which are associated with CML progression and TKI resistance mechanism. K562, a human chronic myleoid cell line, was treated with imatinib in a time and dose dependent manner and cytotoxicity and lncRNAs levels were evaluated. Key words: Chronic myeloid leukemia, long non-coding RNAs, resistance mechanism of tyrosine kinase inhibitor in CML