摘要
细胞因子信号转导抑制因子(SOCS)通过作用于细胞因子信号转导通路(主要是JAK/STAT通路),负反馈调节细胞因子信号转导;而细胞因子信号转导通路又可以调节SOCS的表达,从而形成一个负反馈调节环。在多发性骨髓瘤(MM)的发病机制中,白细胞介素-6(IL-6)是肿瘤细胞生长和生存的一个重要因素。最近,发现SOCS基因的甲基化可以使SOCS失活。SOCS甲基化后导致IL-6信号转导的持续增强,从而支持了MM细胞的生存和增生。
The suppressors ot cytokine signalhng（50CS） negatively regulates signal transduction trom cytokines that act through the signal transduction pathway （particularly the JAK/STAT pathway）,and the signal transduction pathway regulate SOCS gene transcription. Thus a negative feedback loop is completed. In multiple myeloma（MM） pathogenesis, IL-6 has been identified as an essential growth and survival factor. Recently, it is demonstrated that SOCS is frequently silenced by methylation, The methylation of SOCS gene may result in increased IL-6 signal transduction, and thus support survival and expansion of MM cells.
出处
《白血病．淋巴瘤》
CAS
2006年第3期223-225,共3页
Journal of Leukemia & Lymphoma
