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目的初步探讨α/β干扰素抑制淋巴瘤细胞增殖的分子机制。方法用IFN-α/β处理淋巴瘤细胞(Namalwa、JeKo-1)和白血病细胞(Jurkat、THP-1)24 h,CCK-8法检测IFN-α/β对上述细胞的增殖抑制效果;RT-PCR、real-time PCR、Western blot检测其SARI mRNA和蛋白水平的变化;对SARI基因启动子区的转录因子结合位点进行生物信息学预测。结果 IFN-α和IFN-β均可有效杀伤Namalwa和JeKo-1淋巴瘤细胞(P<0.05),且均能显著诱导淋巴瘤细胞SARI mRNA和蛋白的表达(P<0.05),但两种干扰素对Jurkat和THP-1白血病细胞的存活及SARI的表达均无显著影响(P>0.05);生物信息学分析显示,SARI启动子区含有转录因子STAT的结合位点。结论上调SARI表达可能是IFN-α/β抑制淋巴瘤细胞增殖的机制之一,而SARI的上调可能是由STAT介导的。
Objective To investigate the molecular mechanism of α / β interferon inhibiting the proliferation of lymphoma cells. Methods The inhibitory effect of IFN-α / β on the proliferation of the above cells was detected by CCK-8 assay after 24 h treatment of lymphoma cells (Namalwa, JeKo-1) and leukemia cells (Jurkat, THP- The changes of SARI mRNA and protein levels were detected by PCR, real-time PCR and Western blot. The bioinformatics prediction of transcription factor binding sites in SARI gene promoter region was performed. Results Both IFN-α and IFN-β could effectively kill Namalwa and JeKo-1 lymphoma cells (P <0.05), and both of them could significantly induce the expression of SARI mRNA and protein in lymphoma cells (P <0.05) There was no significant difference in survival and SARI expression of Jurkat and THP-1 leukemia cells (P> 0.05). Bioinformatics analysis showed that the SARI promoter region contained the STAT binding site. Conclusion Up-regulation of SARI expression may be one of the mechanisms by which IFN-α / β inhibits the proliferation of lymphoma cells. The upregulation of SARI may be mediated by STAT.