کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10899303 | 1084363 | 2016 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
N-Myc-interacting protein (NMI) negatively regulates epithelial-mesenchymal transition by inhibiting the acetylation of NF-κB/p65
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کلمات کلیدی
NF-κBMYCHDACI-κB kinasemyelocytomatosis oncogeneCBPIKKKAP1IRFNmi - NMISTATs - STATSTip60 - TIP60interferon - اینترفرونIFN - اینترفرون هاEMT - تکنسین فوریتهای پزشکیbreast cancer 1 - سرطان پستان 1IFN regulatory factor - عامل تنظیم کننده IFNnuclear factor kappa-light-chain-enhancer of activated B cells - فاکتور هسته ای kappa-light-chain-enhancer از سلول های B فعال شده استsignal transducers and activators of transcription - مبدل سیگنال و فعال کننده رونویسیHistone acetyltransferase - هیستون استیل ترانسفرازhistone deacetylase - هیستون داستیلازCREB-binding protein - پروتئین اتصال CREBBRCA1 - ژن BRCA1HAT - کلاهEpithelial-mesenchymal transition - گذار اپیتلیال-مزانشیمی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: N-Myc-interacting protein (NMI) negatively regulates epithelial-mesenchymal transition by inhibiting the acetylation of NF-κB/p65 N-Myc-interacting protein (NMI) negatively regulates epithelial-mesenchymal transition by inhibiting the acetylation of NF-κB/p65](/preview/png/10899303.png)
چکیده انگلیسی
The epithelial-mesenchymal transition (EMT) plays an essential role in embryonic development, wound healing, tissue regeneration, organ fibrosis, and tumor progression. However, the mechanisms underlying this process are poorly understood. Many signaling pathways, including the NF-κB signaling pathway, trigger EMT during development and differentiation. In the present study, we report that N-Myc interactor (NMI) inhibits EMT progression by suppressing transcriptional activities of NF-κB in human gastric cancer cells. We show that the expression of NMI is significantly reduced in invasive gastric cancer cells and gastric cancer tissues. Overexpression of NMI inhibited cell migration and invasion, and this inhibition was enhanced after TNF-α stimulation. Tumorigenicity assay in nude mice support the notion that NMI inhibits EMT in cancer cells. Mechanistically, NMI promotes the interaction between NF-κB/p65 and histone deacetylases (HDACs) and inhibits the acetylation and transcriptional activity of p65. The expression of p65 rescues NMI-mediated inhibition of EMT and the inhibition of the acetylation of p65 mediated by NMI is HDACs-dependent. Taken together, these findings suggest that NMI can suppress tumor invasion and metastasis by inhibiting NF-κB pathways, providing an alternative mechanism for EMT inhibition in stomach neoplasm.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cancer Letters - Volume 376, Issue 1, 28 June 2016, Pages 22-33
Journal: Cancer Letters - Volume 376, Issue 1, 28 June 2016, Pages 22-33
نویسندگان
Jingjing Hou, Tao Wang, Qingqing Xie, Weixian Deng, James Y. Yang, Si Qing Zhang, Jian-Chun Cai,