N-Myc-interacting protein (NMI) negatively regulates epithelial-mesenchymal transition by inhibiting the acetylation of NF-κB/p65
详细信息 查看全文
- 作者：Jingjing Houa ; b ; c ; Tao Wanga ; b ; c ; Qingqing Xied ; Weixian Denga ; b ; James Y. Yangd ; Si Qing Zhangd ; zhangsq@xmu.edu.cn" class="auth_mail" title="E-mail the corresponding author ; Jian-Chun Caia ; b ; c ; jianchunfh2@sina.com" class="auth_mail" title="E-mail the corresponding author
- 关键词：BRCA1 ; breast cancer 1 ; CBP ; CREB-binding protein ; EMT ; epithelial-mesenchymal transition ; HAT ; histone acetyltransferase ; HDAC ; histone deacetylase ; IFN ; interferon ; IKK ; I-κB kinase ; KAP1 ; Krü ; ppel-associated box-associated protein ; IRF ; IFN regulatory factor ; Myc ; myelocytomatosis oncogene ; NF-κB ; nuclear factor kappa-light-chain-enhancer of activated B cells ; NMI ; N-Myc and STATs interactor ; STATs ; signal transducers and activators of transcription ; TIP60 ; Tat-interacting protein 60&thin
- 刊名：Cancer Letters
- 出版年：2016
- 出版时间：28 June 2016
- 年：2016
- 卷：376
- 期：1
- 页码：22-33
- 全文大小：2848 K
文摘
- •
We showed that NMI regulates EMT via the NF-κB pathway.
- •
NMI overexpression reduces the invasion and migration of gastric cancer cells.
- •
We found NMI inhibits the transcription activities of NF-κB and overexpression of p65 rescues NMI mediated inhibition of EMT.
- •
NMI promotes the interaction between NF-κB/p65 and HDACs and inhibits the acetylation and transcriptional activity of p65.
- •
Our results provide an alternative mechanism for EMT inhibition and suggest NMI has a critical role in suppressing stomach neoplasm progression.