Department of Internal Medicine: Genetic Medicine, University of Michigan, Ann Arbor, Michigan. Rogel Cancer Center, University of Michigan, Ann Arbor, Michigan.
Cancer Discov. 2020 Jun;10(6):765-767. doi: 10.1158/2159-8290.CD-20-0358.
Although mutations in are the most common RNA-splicing factor mutations in cancer, determining the downstream missplicing events that drive tumorigenesis has remained challenging. Liu and colleagues present a model by which mutant SF3B1 tumors displayed high levels of oncogenic MYC activity through the missplicing of PP2A-B56α, a key post-translational regulator of MYC stability, providing a new therapeutic target and driver of SF3B1-mediated tumorigenesis..
虽然 中的突变是癌症中最常见的 RNA 剪接因子突变，但确定驱动肿瘤发生的下游剪接事件一直具有挑战性。Liu 及其同事提出了一个模型，即突变的 SF3B1 肿瘤通过 PP2A-B56α 的错剪接显示出高水平的致癌 MYC 活性，PP2A-B56α 是 MYC 稳定性的关键翻译后调节因子，为 SF3B1 介导的肿瘤发生提供了新的治疗靶点和驱动因素。
