RBBP6 has been implicated in tumorigenesis but its role in tumor metastasis and progression has not been evaluated. Interestingly, here we show that RBBP6 is upregulated in colorectal cancer (CRC) where its expression level is positively correlated with distant metastasis. In this study, we identified RBBP6, a RING Finger-domain E3 ubiquitin ligase, served as an independent prognostic factor and predicted poor outcome for CRC patients. RBBP6 promoted cell proliferation, migration, and invasion in CRC cells and promoted tumor growth, lung metastasis, and liver metastasis in mouse models. Mechanistically, we revealed that RBBP6 bound and ubiquitylated IκBα, an inhibitor of the NF-κB-signaling pathway. RBBP6-mediated ubiquitination and degradation of IκBα significantly enhanced p65 nuclear translocation, which triggered the activation of NF-κB pathway and then induced the epithelial-mesenchymal transition (EMT) process and cell metastasis. Furthermore, by DNA methylation results and ChIP analysis, we demonstrated that the promoter of RBBP6 was hypomethylated, and was activated by multi-oncogenic transcription factors. In conclusion, our findings suggest that RBBP6 may be a potential prognostic biomarker and therapeutic target for CRC invasion and metastasis.

译文

:RBBP6与肿瘤发生有关,但尚未评估其在肿瘤转移和进展中的作用。有趣的是,在这里我们显示RBBP6在结直肠癌(CRC)中表达上调,其表达水平与远处转移呈正相关。在这项研究中,我们确定了RING指域E3泛素连接酶RBBP6作为独立的预后因素,并预测CRC患者的预后不良。 RBBP6促进了CRC细胞中细胞的增殖,迁移和侵袭,并促进了小鼠模型中的肿瘤生长,肺转移和肝转移。从机理上讲,我们发现RBBP6结合并泛素化了IκBα,即NF-κB信号通路的抑制剂。 RBBP6介导的IκBα泛素化和降解显着增强p65核易位,从而触发NF-κB通路的激活,然后诱导上皮-间质转化(EMT)过程和细胞转移。此外,通过DNA甲基化结果和ChIP分析,我们证明RBBP6的启动子被低甲基化,并被多种致癌转录因子激活。总之,我们的发现提示RBBP6可能是CRC侵袭和转移的潜在预后生物标志物和治疗靶标。

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