H Wu1, J Liu2, Y Zhang3, Q Li4, Q Wang5, Z Gu6. 1. Department of Gynaecology, Jining No.1 People's Hospital, Jining, 272011, People's Republic of China. 2. Department of Obstetrics, The Third People's Hospital of Qingdao, Qingdao, 266041, People's Republic of China. 3. Education Management Section, Qingdao Central Hospital, Qingdao University, Qingdao, 266042, People's Republic of China. 4. Department of Clinical Laboratory, The People's Hospital of Zhangqiu Area, Jinan, 250200, People's Republic of China. 5. No.2 Department of Otorhinolaryngology, The People's Hospital of Zhangqiu Area, Jinan, 250200, People's Republic of China. 6. Department of Obstetrics and Gynecology, The 5th People's Hospital of Ji'nan, 24297 Jingshi Road, Huaiyin District, Jinan, 250022, People's Republic of China. zaipaku94475@163.com.
Abstract
PURPOSE: miR-22 plays a great role in inhibiting cell growth, metastasis and enhanced cell apoptosis in several cancers. The purpose of this study was to investigate the functions of miR-22 in ovarian cancer. METHODS: The proliferative ability was measured using CCK-8 assay. The protein expression associated with EMT and PI3K/AKT signaling biomarkers were measured by western blot. Luciferase assay applied to measure the luciferase activity. Kaplan-Meier method was performed to evaluate the overall survival rate of ovarian cancers. RESULTS: miR-22 was low expressed and NLRP3 was overexpressed in ovarian cancer tissues and cells, and downregulation of miR-22 was associated with poor prognosis. The expression of NLRP3 had a negative correlation with miR-22 expression in ovarian cancer. miR-22 promoted cell viability and EMT through directly binding to the 3'-UTR of NLRP3 mRNA and inhibited PI3K/AKT signaling pathway. NLRP3 partially restored functions of miR-22 on cell proliferation and EMT in ovarian cancer. CONCLUSION: miR-22 impaired cell viability and EMT by NLRP3 and inhibited PI3K/AKT signaling pathway in ovarian cancer. The newly identified miR-22/NLRP3/PI3K/AKT axis provides novel insight into the pathogenesis of ovarian cancer.
PURPOSE:miR-22 plays a great role in inhibiting cell growth, metastasis and enhanced cell apoptosis in several cancers. The purpose of this study was to investigate the functions of miR-22 in ovarian cancer. METHODS: The proliferative ability was measured using CCK-8 assay. The protein expression associated with EMT and PI3K/AKT signaling biomarkers were measured by western blot. Luciferase assay applied to measure the luciferase activity. Kaplan-Meier method was performed to evaluate the overall survival rate of ovarian cancers. RESULTS:miR-22 was low expressed and NLRP3 was overexpressed in ovarian cancer tissues and cells, and downregulation of miR-22 was associated with poor prognosis. The expression of NLRP3 had a negative correlation with miR-22 expression in ovarian cancer. miR-22 promoted cell viability and EMT through directly binding to the 3'-UTR of NLRP3 mRNA and inhibited PI3K/AKT signaling pathway. NLRP3 partially restored functions of miR-22 on cell proliferation and EMT in ovarian cancer. CONCLUSION:miR-22 impaired cell viability and EMT by NLRP3 and inhibited PI3K/AKT signaling pathway in ovarian cancer. The newly identified miR-22/NLRP3/PI3K/AKT axis provides novel insight into the pathogenesis of ovarian cancer.
Authors: Wen Q Li; Ai S Fu; Dong F Shao; Qian Zhang; Meng H Wang; Hong Y Wang; Yi Chen; Ci Zhang; Xiao Y Zhu; Yan L Ge Journal: Clin Lab Date: 2019-10-01 Impact factor: 1.138