The differentially expressed genes profile upon HNRPDL silencing in K562 cells

In our previous study, the roles of heterogeneous nuclear ribonucleoprotein D-like (HNRPDL) in CML cells were revealed. We found that overexpression of HNRPDL transformed murine BaF3 cells and induced lethal mice leukemia. Conversely, HNRPDL silencing inhibited colony-forming cell (CFC) production of CML CD34+ cells and attenuated BCR-ABL induced mice leukemia. In addition, HNRPDL modulated imatinib response of K562 cells and HNRPDL silencing sensitized CML CD34+ cells to imatinib treatment. To obtain molecular insights of how HNRPDL modulates the growth and imatinib response of human CML cells, we generated microarray data comparing HNRPDL silenced K562 cells with control (Scramble) cells. 3 biological replicates of Scramble and HNRPDL silenced K562 cells were harvested for microarray analysis using Agilent whole human genome oligo-chips (4×180K) in Shanghai Biotechnology Corporation. The differentially expressed transcripts were determined based on Student’s t-test (P<0.05) and fold change (>2).