Background: Evidence is accumulating that extracellular microvesicles (MVs) facilitate progression and relapse in cancer.Our previous work demonstrated that MVs derived from K562 chronic myeloid leukemia (CML) cells can transform mononuclear cells (MNCs) from normal hematopoietic transplants to acute leukemia-like cancer cells.This transformation model provides an opportunity to explore the mechanism of blast crisis (BC) of CML and the occurrence of donor cell leukemia.However,the transformation mechanisms are still poorly understood.Here,we use gene expression studies and network analyses to elucidate the key factors and exploring their regulatory mechanisms of our model,which will shed light on the leukemogenesis and transformation of CML.Methods: We did RNA-seq and small RNA-seq for samples of the critical transformation points.Differentially expressed analysis were performed for genes,TFs and miRNAs.Then,the differentially expressed sets were filtered by cancer-related pathway,fold change,expression level and so on.At last,we construct TF-miRNA co-regulatory network for the differentially expressed genes,TFs and miRNAs to illuminate the dysregulatory mechanism of the transformation.