The role of CML28 in regulation of proliferation and apoptosis of K562 cells
BAI Xueling1,2,MAO Xia1,ZHANG Bing1,CAO Fengbin2,and ZHANG Donghua1.
1. Department of Hematology, Tongji Hospital affiliated to Tongji Medical College, Huazhong University of Science ＆ Technology. Wuhan 430030，China; 2.Medical Team of Luoyang Military Detachment, Henan Provincial Corps, Chinese Armed Police Forces, Luoyang 471000，China
Abstract：Objective To explore the role of CML28 in regulation of proliferation and apoptosis of K562 cells. Methods K562 cells were cultured in vitro and electrotransfected with Si-hCML28. K562 cells which had been transfected were collected after 48 hours. Total mRNA was extracted from K562 cells using Trizol reagent and the first cDNA was synthesized using the reverse transcription kit.The silence effect was detected by RT-PCR and Real time PCR. The ratio of apoptosis and proliferation of K562 cells was detected by Flow Cytometry (FCM)after CML28 was down-regulated. Data were analyzed by SPSS17.0 statistics software and P <0.05 was considered statistically significant. Results (1) There was a high level of CML28 in K562 cells; (2)The mRNA expression of CML28 was 0.524 ± 0.044 after interference, lower than that of negative control. There was statistically significant difference；(3) The apoptosis ratio was (22.45±3.54)% in the group of Si-hCML28, higher than that of negative control. Conclusions CML28 is highly expressed in K562 cells. The mRNA expression of CML28 can be effectively down-regulated by Si-hCML28. In addition, it can significantly inhibit K562 cell proliferation and induce apoptosis of K562 cells, suggesting that it plays an important role in regulating the apoptosis and proliferation of K562 cells.
白雪玲,毛 霞,张 冰,曹丰斌,张东华. CML28在K562细胞增殖与凋亡调控中的作用研究[J]. 武警医学, 2012, 23(8): 678-678.
BAI Xueling,MAO Xia,ZHANG Bing,CAO Fengbin,and ZHANG Donghua.. The role of CML28 in regulation of proliferation and apoptosis of K562 cells. Med. J. Chin. Peop. Armed Poli. Forc., 2012, 23(8): 678-678.
Yang XF, Wu CJ, Chen L, et al. CML28 is a broadly immunogenic antigen, which is overexpressed in tumor cells ［J］. Cancer Res， 2002, 62(19):5517-5522.［2］ Zhou H, Zhang D, Wang Y, et al. Induction of CML28-specific cytotoxic T cell responses using co-transfected dendritic cells with CML28 DNA vaccine and SOCS1 small interfering RNA expression vector ［J］. Biochem Biophys Res Commun， 2006, 347(1):200-207. ［3］ Zhang DH, Zhou HS, Wang YY, et al. Construction and expression of dendritic cell nucleic acid vaccine containing CML28 gene in human dendritic cells ［J］.Zhongguo Shi Yan Xue Ye Xue Za Zhi, 2005, 13(4):631-636.［4］ Anderson JS, Parker RP. The 3’to 5’degradation of yeast mRNAs is a general mechanism for mRNA turnover that requires the SKI2 DEVH box protein and 3’ to 5’exonucleases of the exosome complex ［J］. EMBO J, 1998, 17(5):1497-1506.［5］ 萨仁高娃,吴岩,肖文华. EXOSOME与肿瘤免疫治疗的研究进展［J］.感染、炎症、修复，2008, 9（3）：181-184.
2012, Vol. 23 
