6BIO通过JAK1-STAT3信号转导通路抑制小鼠B16恶性黑色素瘤细胞的增殖

6BIO inhibits the proliferation of mouse B16 melanoma cells through JAK1 -STAT3 signaling pathway

目的研究（2’Z，3’E）-6-溴靛玉红-3’-肟衍生物（6BIO）对小鼠B16恶性黑色素瘤细胞增殖能力的影响。方法免疫组化法检测6BIO处理不同时间（24、36、48h）后B16细胞增殖指数Ki67的表达；Western blot法检测6BIO处理不同时间（1、6、12、24h）后B16细胞中磷酸化JAK激酶1蛋白（p-JAK1）和磷酸化信号转录子和转录激活子3蛋白（p-STAT3）的表达。结果6BIO处理不同时间后B16细胞增殖指数Ki67的表达均呈时间依赖性降低（P〈0．01）。6BIO能够时间依赖性抑制B16细胞中p-JAK1和p—STAT3蛋白的表达（P〈0．01）。结论6BIO能够通过抑制JAK1-STAT3信号转导通路抑制小鼠B16恶性黑色素瘤细胞的增殖。

Objective To investigate the influence of 6 - bromoindirubin - 3′ - oxime （6BIO） on the proliferation of mouse B16 melanoma cells. Methods Immunohistochemical method was used to detect the change of Ki67 proliferation index in B16 cells after they were treated with 6BIO for different time durations （24, 36, and 48 h） ; Western blot analysis was used to detect the phosphorylation level of Janus protein tyrosin kinase 1 （p- JAK1 ） and signal transducers and activators of transcrpition 3 （ p - STAT3 ） in B16 cells after they were treated with 6BIO for different time durations （ 1,6, 12, and 24 h）. Results After treated with 6BIO for different time durations, Ki67 proliferation index in B16 cells was decreased in a time - dependent manner （ P 〈 0.01 ）. 6BIO inhibited the expression of p - JAK1 and p - STAT3 protein in B16 cells in a time - dependent manner （ P 〈 0.01 ）. Conclusion 6BIO inhibits the proliferation of mouse B16 melanoma cells through the JAK1 - STAT3 signaling pathway.