circCTIC1 通过依赖于 BPTF 的 c-Myc 表达促进结肠 TIC 自我更新。
circCTIC1 promotes the self-renewal of colon TICs through BPTF-dependent c-Myc expression.
机构信息
Department of Colorectal Surgery, Affiliated Hospital of Guizhou Medical University, Gui Zhou Province, Guiyang, China.
Guizhou Medical University, Gui Zhou Province, Guiyang, China.
出版信息
Carcinogenesis. 2019 Jun 10;40(4):560-568. doi: 10.1093/carcin/bgy144.
Colon tumor is a conman tumor in the world. There are various kinds of cells in colon tumor bulk, and only a small population can initiate tumor efficiently and termed as tumor-initiating cells (TICs). With self-renewal and differentiation capacities, colon TICs drive colon tumorigenesis, metastasis and relapse. However, the molecular mechanisms of colon TICs self-renewal are elusive. Here, we found that circular RNA (circCTIC1) was highly expressed in colon tumor and colon TICs. circCTIC1 knockdown impaired the self-renewal of colon TICs, and its overexpression played an opposite role. circCTIC1 promoted the expression of c-Myc and drove the self-renewal of colon TIC through c-Myc-dependent manner. circCTIC1 interacted with nuclear remodeling factor (NURF) complex, recruited NURF complex onto c-Myc promoter and finally drove the transcriptional initiation of c-Myc. Altogether, circCTIC1 drove the self-renewal of colon TICs through bromodomain PHD finger transcription factor (BPTF)-mediated c-Myc expression.
结肠肿瘤是一种世界性的骗子肿瘤。结肠肿瘤块中有各种细胞，只有一小部分能够有效地启动肿瘤，被称为肿瘤起始细胞（TICs）。结肠 TICs 具有自我更新和分化能力，驱动结肠肿瘤发生、转移和复发。然而，结肠 TICs 自我更新的分子机制尚不清楚。在这里，我们发现环状 RNA（circCTIC1）在结肠肿瘤和结肠 TICs 中高度表达。circCTIC1 敲低削弱了结肠 TICs 的自我更新能力，而过表达则起到相反的作用。circCTIC1 通过 c-Myc 依赖性途径促进 c-Myc 的表达，从而驱动结肠 TIC 的自我更新。circCTIC1 与核重塑因子（NURF）复合物相互作用，将 NURF 复合物募集到 c-Myc 启动子上，最终驱动 c-Myc 的转录起始。总之，circCTIC1 通过溴结构域 PH 结构域转录因子（BPTF）介导的 c-Myc 表达驱动结肠 TICs 的自我更新。
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