title: IL-17A promotes the migration and invasiveness of cervical cancer cells by coordinately activating MMPs expression via the p38/NF-κB signal pathway.
abstract: OBJECTIVE
  IL-17A plays an important role in many inflammatory diseases and cancers. We aimed to examine the effect of IL-17A on the invasion of cervical cancer cells and study its related mechanisms.
  
  
  METHODS
  Wound healing and matrigel transwell assays were used to examine the effect of IL-17A on cervical cancer cell migration and invasion by a panel of cervical cancer cell lines. The levels of matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases (TIMPs) were investigated using western blotting. The activity of p38 and nuclear factor-kappa B (NF-κB) signal pathway was detected too.
  
  
  RESULTS
  Here, we showed that IL-17A could promote the migration and invasion of cervical cancer cells. Further molecular analysis showed that IL-17A could up-regulate the expressions and activities of MMP2 and MMP9, and down-regulate the expressions of TIMP-1 and TIMP-2. Furthermore, IL-17A also activates p38 signal pathway and increased p50 and p65 nuclear expression. In addition, treatment of cervical cancer cells with the pharmacological p38/NF-κB signal pathway inhibitors, SB203580 and PDTC, potently restored the roles of invasion and upregulation of MMPs induced by IL-17A.
  
  
  CONCLUSIONS
  IL-17A could promote the migration and invasion of cervical cancer cell via up-regulating MMP2 and MMP9 expression, and down-regulating TIMP-1 and TIMP-2 expression via p38/NF-κB signal pathway. IL-17A may be a potential target to improve the prognosis for patients with cervical cancer.
authors.affiliation: Department of Obstetrics and Gynaecology, Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, P. R. China.
authors.forename: Minjuan
authors.initials: M
authors.lastname: Feng
authors.affiliation: Department of Obstetrics and Gynaecology, Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, P. R. China.
authors.forename: Yidong
authors.initials: Y
authors.lastname: Wang
authors.affiliation: School of Medicine, Xi'an Jiaotong University, Xi'an, P. R. China.
authors.forename: Kunlun
authors.initials: K
authors.lastname: Chen
authors.affiliation: Department 5 of Rheumatology, The Fifth Hospital of Xi'an City, Xi'an, P. R. China.
authors.forename: Zhuoqiong
authors.initials: Z
authors.lastname: Bian
authors.affiliation: Department of Obstetrics and Gynaecology, Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, P. R. China.
authors.lastname: Jinfang Wu
authors.affiliation: Department of Obstetrics and Gynaecology, Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, P. R. China.
authors.forename: Qing
authors.initials: Q
authors.lastname: Gao
mesh_terms: D000328:Adult; D045744:Cell Line, Tumor; D005260:Female; D006801:Humans; D020381:Interleukin-17 / Q000502:physiology*; D020782:Matrix Metalloproteinases / Q000378:metabolism*; D008875:Middle Aged; D016328:NF-kappa B / Q000378:metabolism*; D009361:Neoplasm Invasiveness; D009362:Neoplasm Metastasis; D002583:Uterine Cervical Neoplasms / Q000201:enzymology / Q000378:metabolism / Q000473:pathology*; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism*
chemical_list: D020381:Interleukin-17; D016328:NF-kappa B; D048051:p38 Mitogen-Activated Protein Kinases; D020782:Matrix Metalloproteinases