RT Journal Article
SR Electronic
T1 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
JF International Journal of Gynecologic Cancer
JO Int J Gynecol Cancer
FD BMJ Publishing Group Ltd
SP 1533
OP 1539
DO 10.1097/IGC.0b013e31822d2abd
VO 21
IS 9
A1 Ting Lai
A1 Kana Wang
A1 Qiannan Hou
A1 Jian Zhang
A1 Jialing Yuan
A1 Lixing Yuan
A1 Zongbing You
A1 Mingrong Xi
YR 2011
UL http://ijgc.bmj.com/content/21/9/1533.abstract
AB Objectives 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.Conclusion These results demonstrated that IL-17 may regulate chemokines and cytokines in gynecologic cancers.