Huang Qing, Yang Yan, Li Xiaoqing, Huang Shiang
Center for Stem Cell Research and Application, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Tumour Biol. 2011 Dec;32(6):1191-7. doi: 10.1007/s13277-011-0222-1. Epub 2011 Sep 3.
The BCR-ABL tyrosine kinase has been implicated in the dysregulation of oncogenes and tumor suppressor genes involved in chronic myelogenous leukemia (CML). Suppressor of activator protein-1, regulated by interferon (SARI), is a recently identified tumor suppressor gene whose expression has been reported to be suppressed in several malignant neoplasms. However, the expression of SARI in leukemia and the underlying regulatory mechanism remain elusive. In this study, we demonstrated that SARI mRNA expression was low in CML patients. In vitro, BCR-ABL kinase inhibitor imatinib mesylate or siRNA specific to BCR-ABL upregulated SARI mRNA expression in human leukemia cells. In addition, JAK/STAT signaling inhibitor AG490 and RAS/MAPK signaling inhibitor PD98059 upregulated SARI mRNA expression, but PI3K/AKT pathway inhibitor LY294002 had no such effect. Functionally, silencing of SARI in CML-derived cell line K562 partially decreased imatinib mesylate-induced apoptosis. Taken together, these data demonstrate that SARI mRNA expression is suppressed by BCR-ABL through the downstream signaling pathways, suggesting SARI as a potential therapeutic target in CML.
BCR-ABL酪氨酸激酶与慢性粒细胞白血病(CML)中癌基因和肿瘤抑制基因的失调有关。干扰素调节的激活蛋白-1抑制因子(SARI)是最近发现的一种肿瘤抑制基因,据报道其表达在几种恶性肿瘤中受到抑制。然而,SARI在白血病中的表达及其潜在的调控机制仍不清楚。在本研究中,我们证明CML患者中SARI mRNA表达较低。在体外,BCR-ABL激酶抑制剂甲磺酸伊马替尼或针对BCR-ABL的小干扰RNA(siRNA)可上调人白血病细胞中SARI mRNA的表达。此外,JAK/STAT信号抑制剂AG490和RAS/MAPK信号抑制剂PD98059可上调SARI mRNA的表达,但PI3K/AKT途径抑制剂LY则无此作用。在功能上,CML来源的细胞系K562中SARI的沉默部分降低了甲磺酸伊马替尼诱导的细胞凋亡。综上所述,这些数据表明SARI mRNA的表达受到BCR-ABL通过下游信号通路的抑制,提示SARI可能是CML的一个潜在治疗靶点。