期刊
EXPERIMENTAL AND TOXICOLOGIC PATHOLOGY
卷 69, 期 6, 页码 402-407出版社
ELSEVIER GMBH
DOI: 10.1016/j.etp.2017.03.006
关键词
Nicotine; PI3k/Akt pathway; NF-kappa B pathway; HeLa; Migration; Invasion
资金
- National Natural Science Foundation of China [81300885, 81402150]
- Shandong Provincial key research and development program [2015GSF118122, 2016GSF201115, 2016GSF201220]
- Young Scholars Program of Shandong University [2015WLJH53]
- Construction Engineering Special Fund of Taishan Scholars [ts201511106]
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/Altt and NF kappa-13 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-kappa 8 activation and up regulation of Vimentin. Inhibition of NF-kappa B 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-kappa B pathway in vitro.
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