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Downregulation of N-myc Interactor Promotes Cervical Cancer Cells Growth by Activating Stat3 Signaling
Cell Biochemistry and Biophysics ( IF 1.8 ) Pub Date : 2020-10-27 , DOI: 10.1007/s12013-020-00943-0
Songbin Wu 1, 2, 3 , Xiaotian Li 1 , Huizi Chai 1 , Linyuan Feng 1 , Wenjing Li 1 , Hongjian Li 1
Affiliation  

N-myc interactor (NMI), a member of the oncogene Myc family, has been reported to be closely related to the development of cancer. However, the character of NMI in cervical carcinoma has not been reported. Herein, we found that downregulation of NMI protein not only promoted the proliferation, migration, and invasion of HeLa cells, but also decreased their expression of Caspase-3 and Caspase-9. Silencing NMI promotes the epithelial-mesenchymal transition of human cervical carcinoma HeLa cells by upregulating N-cadherin, vimentin, and downregulating E-cadherin. Further investigation illustrated the downregulation of NMI can activate the STAT3 signaling pathway. In conclusion, we found that the downregulation of NMI plays an important role in the progression of cervical cancer, and may served as a novel therapeutic target for cervical cancer.



中文翻译:

N-myc相互作用因子的下调通过激活Stat3信号传导促进宫颈癌细胞的生长

据报道,癌基因Myc家族成员N-myc相互作用子(NMI)与癌症的发展密切相关。但是,尚未报道宫颈癌中NMI的特征。在本文中,我们发现NMI蛋白的下调不仅促进HeLa细胞的增殖,迁移和侵袭,而且降低其Caspase-3和Caspase-9的表达。沉默NMI通过上调N-钙粘蛋白,波形蛋白和下调E-钙粘蛋白来促进人宫颈癌HeLa细胞的上皮-间质转化。进一步的研究表明NMI的下调可以激活STAT3信号通路。总之,我们发现NMI的下调在宫颈癌的进展中起着重要作用,并且可以作为宫颈癌的新型治疗靶点。

更新日期:2020-10-30
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