title: Interleukin 17 induces up-regulation of chemokine and cytokine expression via activation of the nuclear factor κB and extracellular signal-regulated kinase 1/2 pathways in gynecologic cancer cell lines.
abstract: OBJECTIVE
  Previous studies have revealed that interleukin 17 (IL-17) contributes to pathological processes in many solid tumors. However, the roles of IL-17 in gynecologic cancer still remain elusive, hindering the deep understanding of gynecologic tumorigenesis.
  
  
  METHODS
  In the present study, to delineate the functional roles of IL-17 in gynecologic cancer, IL-17 stimulation was introduced in cell lines of 3 gynecologic cancers, and IL-17-induced expression of chemokines and cytokines and possible signaling pathways were investigated.
  
  
  RESULTS
  Our results showed that in HEC-1-B (human endometrial cancer) cells, IL-17 stimulation induced mRNA level increases of CCL2, CCL5, CCL20, CXCL2, and IL-8. Similar treatment in HeLa cells caused increases in the mRNA levels of CCL2, CXCL2, IL-6, and IL-8, and in SKOV3 cells, mRNA levels of CCL2, CCL20, CXCL1, CXCL2, IL-6, and IL-8 increased. The increases in mRNA levels induced by IL-17 were dose- and time-dependent. Furthermore, with the addition of the NF-κB (nuclear factor κ-light-chain-enhancer of activated B) and extracellular signal-regulated kinase inhibitors pyrrolidine dithiocarbamate and PD98059, the IL-17-induced CCL2 mRNA level was significantly compromised. IL-17 stimulation also activated phosphorylation of IκBα and extracellular signal-regulated kinase 1/2 in a time-dependent manner.
  
  
  CONCLUSIONS
  These results demonstrated that IL-17 may regulate chemokines and cytokines in gynecologic cancers.
authors.affiliation: Department of Gynecology and Obstetrics, West China Second University Hospital, Sichuan University, Sichuan, China.
authors.forename: Ting
authors.initials: T
authors.lastname: Lai
authors.forename: Kana
authors.initials: K
authors.lastname: Wang
authors.forename: Qiannan
authors.initials: Q
authors.lastname: Hou
authors.forename: Jian
authors.initials: J
authors.lastname: Zhang
authors.forename: Jialing
authors.initials: J
authors.lastname: Yuan
authors.forename: Lixing
authors.initials: L
authors.lastname: Yuan
authors.forename: Zongbing
authors.initials: Z
authors.lastname: You
authors.forename: Mingrong
authors.initials: M
authors.lastname: Xi
mesh_terms: D048708:Cell Growth Processes / Q000187:drug effects; D045744:Cell Line, Tumor; D018925:Chemokines / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism; D016207:Cytokines / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism; D005260:Female; D005833:Genital Neoplasms, Female / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D006367:HeLa Cells; D006801:Humans; D020381:Interleukin-17 / Q000378:metabolism / Q000494:pharmacology*; D020935:MAP Kinase Signaling System / Q000187:drug effects; D019950:Mitogen-Activated Protein Kinase 1 / Q000037:antagonists & inhibitors / Q000378:metabolism*; D048052:Mitogen-Activated Protein Kinase 3 / Q000037:antagonists & inhibitors / Q000378:metabolism*; D016328:NF-kappa B / Q000378:metabolism / Q000494:pharmacology; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D013268:Stimulation, Chemical; D015854:Up-Regulation / Q000187:drug effects
chemical_list: D018925:Chemokines; D016207:Cytokines; D020381:Interleukin-17; D016328:NF-kappa B; D012333:RNA, Messenger; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3