Interleukin‐33 predicts poor prognosis and promotes ovarian cancer cell growth and metastasis through regulating ERK and JNK signaling pathways

• DOI: 10.1016/j.molonc.2015.06.004
• Publication Date: 2015-09-08T21:16:26Z
• Authors: Xiaoguang Tong; Mark Barbour; Kezuo Hou; Chao Gao; Shuang Cao; Jingli Zheng; Yang Zhao; Rong Mu; Hui-Rong Jiang
• Keywords: Ovarian Neoplasms; 570; MAP Kinase Signaling System; 610; Receptors, Cell Surface; Interleukin-33; Prognosis; Interleukin-1 Receptor-Like 1 Protein; RS; 3. Good health; 03 medical and health sciences; Pharmacy and materia medica; 0302 clinical medicine; Gene Knockdown Techniques; Humans; Female; Neoplasm Invasiveness; Neoplasm Metastasis; RNA, Small Interfering; Protein Kinase Inhibitors; Cell Proliferation

Epithelial ovarian cancer (EOC) is the most lethal gynecological cancer, it remains a huge challenge to understand cellular and molecular mechanisms of aggressive behavior EOC cells. Here we investigated role an immunomodulatory cytokine IL‐33 its receptor ST2 in mediating growth metastasis EOC. Our data show that both were highly up‐regulated tumors compared with normal ovary benign tumors, expression levels further increased tumor tissues at metastatic site. The positively correlated Ki‐67 expression, negatively patient survival time. Using cell lines, observed cells knocked down gene by siRNA had reduced migratory invasive potential, while full length human (fl‐hIL‐33) promoted invasive, proliferative capacity this process could be inhibited decoy sST2. Signaling pathway analysis suggested phosphorylation ERK JNK which was blocked Fl‐hIL‐33‐induced increases migration, potential proliferation specifically abrogated treatment inhibitor U0126 SP600125 only disrupted IL‐33‐induced enhancement viability. Taken together, our suggest IL‐33/ST2 axis closely associates poor prognosis patients, promotes through regulating signaling pathways. Thus might markers therapeutic targets for patients.