摘要
目的 探讨自细胞介素-24（又称黑色素瘤分化相关基因-7,IL-24/mda-7）对白血病细胞系K562的周期阻滞作用机制.方法 利用基因芯片技术初步分析转染IL-24/mda-7与转染空载体的K562细胞之间基因表达差异,并以实时定量PCR验证;以Western blotting方法检测pRb的磷酸化水平.结果 转染IL-24/mda-7可使K562细胞的细胞周期相关基因p21^WAF-1、BCCIP上调,cdk6、Smurf2下调,定量PCR证实了上述表达变化;IL-24/mda-7转染还可明显降低K562细胞pRb磷酸化水平.结论 IL-24/mda-7可能通过调节细胞周期相关蛋白,即上调p21^WAF-1、BCCIP,下调cdk6、Smurf2,使K562阻滞于G0/G1期,从而抑制细胞生长.
Objective To explore the mechanism of the cell-cycle arrest induced by human melanoma differentiation associated gene-7 （mda-7/IL-24） in chronic myelocytic leukemia cell line K562. Methods Microarray analysis was performed to determine the genes that were differentially regulated by mda-7/IL-24 in K562 cells, and was validated by realtime PCR. The phosphorylated pRb were detected by Western blotting analysis. Results A microarray analysis showed that G0/G1 phase-associated genes p21^WAF-1 and BCCIP were up-egulated, while cdk6 and Smurf2 were down-regulated. The directional change in the expression of the four genes was successfully validated with real-time quantitative RT-PCR. pRb Set^795 phosphorylation was observed with no modification of the pRb protein level. Conclusion These results suggest that IL-24/mda-7 may inhibit K562 proliferation and induce G0/G1 cell cycle angst by up-regulating p21^WAF-1 and BCCIP, down-regulating cdk6 and Smurf2.
出处
《白血病．淋巴瘤》
CAS
2010年第3期133-135,共3页
Journal of Leukemia & Lymphoma
基金
国家自然科学基金（30872983,30672364）
