Literature DB >> 28385482

Nicotine promotes cervical carcinoma cell line HeLa migration and invasion by activating PI3k/Akt/NF-κB pathway in vitro.

Chengze Wang1, Weiting Gu2, Yunpeng Zhang1, Yawen Ji1, Yong Wen3, Xin Xu4.   

Abstract

Cigarette smoking is one of highly risk factors of cervical cancer. Recently nicotine has been reported to increase proliferation and invasion in some smoking related cancers, like non-small cell lung cancer and esophageal squamous cell cancer. However, the effects and mechanisms of nicotine stimulation on cervical cancer cells are not clear. Here, we investigated the effects and mechanisms of nicotine stimulation on HeLa cells in vitro. In our study, we found that nicotine could accelerate HeLa cells migration and invasion, activate PI3K/Akt and NF-κB pathways and increase the expression of Vimentin in vitro. Moreover, we demonstrated that the specific PI3K inhibitor LY294002 could reverse nicotine-induced cell migration and invasion, NF-κB activation and up-regulation of Vimentin. Inhibition of NF-κB by Pyrrolidine dithiocarbamate (PDTC) also antagonized nicotine-induced cell migration, invasion and up-regulation of Vimentin. Simply put, these findings suggest that nicotine promotes cervical carcinoma cell line HeLa migration and invasion by activating PI3k/Akt/NF-κB pathway in vitro.
Copyright © 2017 Elsevier GmbH. All rights reserved.

Entities:  

Keywords:  HeLa; Invasion; Migration; NF-κB pathway; Nicotine; PI3k/Akt pathway

Mesh:

Substances:

Year:  2017        PMID: 28385482     DOI: 10.1016/j.etp.2017.03.006

Source DB:  PubMed          Journal:  Exp Toxicol Pathol        ISSN: 0940-2993


  11 in total

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