CAJ | 학술논문

目的探讨JAK/STATs通路在IL-6信号转导中的功能。方法将含起始密码子在内的约1.2kb STAT3 cDNA反向插入到真核细胞表达载体pcDNA3中，采用电穿孔法将重组质粒导入到M1小鼠急性髓系白血病细胞中，进行G418筛选。结果 G418筛选出抗性克隆后，基因组DNA PCR扩增表明STAT3反义基因片段已导入M1细胞中并在基因组中整合。STAT3反义RNA不影响M1细胞的生长动力学特征，但可显著拮抗IL-6诱导的STAT3激活，并拮抗IL-6对M1细胞的生长抑制效应。结论 STAT3反义RNA能够在M1细胞中稳定表达，成为进一步研究JAK/STATs途径功能的新模型。
목적탐토JAK/STATs통로재IL-6신호전도중적공능。방법장함기시밀마자재내적약1.2kb STAT3 cDNA반향삽입도진핵세포표체재체pcDNA3중，채용전천공법장중조질립도입도M1소서급성수계백혈병세포중，진행G418사선。결과 G418사선출항성극륭후，기인조DNA PCR확증표명STAT3반의기인편단이도입M1세포중병재기인조중정합。STAT3반의RNA불영향M1세포적생장동역학특정，단가현저길항IL-6유도적STAT3격활，병길항IL-6대M1세포적생장억제효응。결론 STAT3반의RNA능구재M1세포중은정표체，성위진일보연구JAK/STATs도경공능적신모형。
Objective　To investigate the biological roles of JAK-STATs pathway in the signal transduction induced by IL-6. Methods　STAT3 antisense expression vector was constructed. The recombinant vector (pST/Fan) or the vector alone (pcDNA3) was transfected into M1 leukemia cells with electroporation technique. Following selection with neomycin, resistant colonies were obtained. The activation of STAT3 induced by IL-6 was analyzed. Results　STAT3 antisense RNA antagonized the IL-6-induced activation of STAT3 efficiently and reduced the inhibitory effect of IL-6 on the growth of M1 cells. However, STAT3 antisense RNA itself did not change the kinetic characteristics of M1 cells. Conclusion　The STAT3 antisense RNA-modified M1 cells may be new model for studying the function of JAK-STATs pathway.