title: Nicotine promotes cervical carcinoma cell line HeLa migration and invasion by activating PI3k/Akt/NF-κB pathway in vitro.
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.
authors.affiliation: School of Stomatology, Shandong University, PR China; Shandong Provincial Key Laboratory of Oral Tissue Regeneration, PR China.
authors.forename: Chengze
authors.initials: C
authors.lastname: Wang
authors.affiliation: Qilu hospital of Shandong University, PR China.
authors.forename: Weiting
authors.initials: W
authors.lastname: Gu
authors.affiliation: School of Stomatology, Shandong University, PR China; Shandong Provincial Key Laboratory of Oral Tissue Regeneration, PR China.
authors.forename: Yunpeng
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: School of Stomatology, Shandong University, PR China; Shandong Provincial Key Laboratory of Oral Tissue Regeneration, PR China.
authors.forename: Yawen
authors.initials: Y
authors.lastname: Ji
authors.affiliation: School of Stomatology, Shandong University, PR China; Shandong Provincial Key Laboratory of Oral Tissue Regeneration, PR China. Electronic address: wenyong@sdu.edu.cn.
authors.forename: Yong
authors.initials: Y
authors.lastname: Wen
authors.affiliation: School of Stomatology, Shandong University, PR China; Shandong Provincial Key Laboratory of Oral Tissue Regeneration, PR China. Electronic address: xinxu@sdu.edu.cn.
authors.forename: Xin
authors.initials: X
authors.lastname: Xu
mesh_terms: D002465:Cell Movement / Q000187:drug effects*; D005260:Female; D006367:HeLa Cells; D006801:Humans; D016328:NF-kappa B / Q000187:drug effects / Q000378:metabolism; D009361:Neoplasm Invasiveness / Q000473:pathology; D009538:Nicotine / Q000633:toxicity*; D019869:Phosphatidylinositol 3-Kinases / Q000187:drug effects / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000187:drug effects / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*; D002583:Uterine Cervical Neoplasms / Q000473:pathology*
chemical_list: D016328:NF-kappa B; D009538:Nicotine; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt
keywords: HeLa; Invasion; Migration; NF-κB pathway; Nicotine; PI3k/Akt pathway