MiR-30e induces apoptosis and sensitizes K562 cells to imatinib treatment via regulation of the BCR-ABL protein.

摘要: Chronic myeloid leukemia (CML) is a disorder of hematopoietic stem cell carrying the Philadelphia (Ph) chromosome and an oncogenic BCR-ABL fusion gene. Tyrosine kinase inhibitors (TKIs) are treatment choice for CML patients. Imatinib was first TKI used in clinical practice with excellent results. MicroRNAs (miRNAs) short non-coding regulatory RNAs that control gene expression play important role cancer development progression. Aberrant miRNA profiles have been shown to be characteristic many cancers. Here, we demonstrate miR-30e expressed at low levels lines patient samples. Bioinformatics analysis reveals putative target site 3'-untranslated region (UTR) ABL In agreement, luciferase assay verified directly targets ABL. Enforced K562 cells suppressed proliferation induced apoptosis these sensitized them imatinib treatment. These findings strongly suggest acts as tumor suppressor by downregulating expression. Up-regulation may therefore therapeutic efficacy against this disease.