标题:NFKB1-miR-612-FAIM2 pathway regulates tumorigenesis in neurofibromatosis type 1
作者:Wang, Meng; Wang, Zengtao; Zhu, Xiaolei; Guan, Shibing; Liu, Zhibo
作者机构:[Wang, Meng; Wang, Zengtao; Zhu, Xiaolei; Guan, Shibing; Liu, Zhibo] Shandong Univ, Hand & Foot Surg Ctr, Prov Hosp, Jinan 250021, Shandong, Peoples R 更多
通讯作者:Wang, M
通讯作者地址:[Wang, M]Shandong Univ, Hand & Foot Surg Ctr, Prov Hosp, Jinan 250021, Shandong, Peoples R China.
来源:IN VITRO CELLULAR & DEVELOPMENTAL BIOLOGY-ANIMAL
出版年:2019
卷:55
期:7
页码:491-500
DOI:10.1007/s11626-019-00370-3
关键词:NF1; MPNST; miR-612; NFKB1; FAIM2
摘要:Neurofibromatosis type I (NF1) is a carcinoma mainly featured by malignant peripheral nerve sheath tumor (MPNST). Dysregulated microRNAs (miRNAs) play decisive roles in tumor initiation and development. Our study sought for the possible roles of miR-612 in NF1. RT-qPCR estimated the expression of nuclear factor kappa B subunit 1 (NFKB1), miR-612, and Fas apoptotic inhibitory molecule 2 (FAIM2) in NF1, separately. Cell proliferation and migration were detected by CCK-8 and transwell experiments. Cell apoptosis was measured via flow cytometry and detection of the expression and activity of caspase 3/8/9. Luciferase reporter, ChIP, and RIP assays testified the interplay between studied genes. Rescue and in vivo assays affirmed the whole mechanism of miR-612 in NF1. We indicated that miR-612 was significantly low in tumor tissues and cells. Mechanism experiments confirmed that miR-612 promotion repressed cell proliferation and migration, and induced cell apoptosis. Besides, NFKB1-regulated miR-612 targeted FAIM2. Spearman's correlation analysis validated the correlation between each two genes. Finally, rescue and in vivo assays affirmed that miR-612 targeted FAIM2 to regulate cellular activities of NF1. The current investigation uncovered the molecular mechanism underlying miR-612 in NF1, establishing miR-612 as a novel therapeutic target for the treatment of NF1 patients.
收录类别:SCOPUS;SCIE
资源类型:期刊论文
原文链接:https://www.scopus.com/inward/record.uri?eid=2-s2.0-85067899353&doi=10.1007%2fs11626-019-00370-3&partnerID=40&md5=2e5b4c75e7542b1ad9da253c67c7d1bc
TOP