2. Academic Validation
  3. Downregulation of N-myc Interactor Promotes Cervical Cancer Cells Growth by Activating Stat3 Signaling

Downregulation of N-myc Interactor Promotes Cervical Cancer Cells Growth by Activating Stat3 Signaling

  • Cell Biochem Biophys. 2021 Mar;79(1):103-111. 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 4
Affiliations

Affiliations

  • 1 Department of Biotechnology, College of Life Science and Technology, Jinan University, Guangzhou, Guangdong, China.
  • 2 Department of Pain Medicine, Huazhong University of Science and Technology Union Shenzhen Hospital (Nanshan Hospital), Shenzhen, China.
  • 3 Shenzhen Key Laboratory of Pain Medicine, Nanshan Hospital, Shenzhen, China.
  • 4 Department of Biotechnology, College of Life Science and Technology, Jinan University, Guangzhou, Guangdong, China. tlihj@jnu.edu.cn.
PMID: 33106998 DOI: 10.1007/s12013-020-00943-0
Abstract

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.

Keywords

Apoptosis; EMT; NMI; Proliferation; Stat3 signaling pathway.

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