title: Downregulation of LRIG1 expression by RNA interference promotes the             aggressive properties of glioma cells via EGFR/Akt/c-Myc activation.
abstract: The LRIG1 [leucine-rich repeats and immunoglobulin-like domains (LRIG)]             gene is not universally downregulated in human cancers, and its role in tumorigenesis             and the development of glioma has not been well addressed. In this study, we used             short hairpin RNA (shRNA)-triggered RNA interference (RNAi) to block LRIG1 gene             expression in the GL15 human glioma cell line. Specific downregulation of LRIG1             by shRNA resulted in significantly enhanced capabilities of proliferation, inhibition             of apoptosis and invasion in the GL15 cells. LRIG1 repression induced marked activation             of epidermal growth factor receptor (EGFR), protein kinase B (Akt) and c-Myc signaling             molecules. Our results demonstrated that RNAi against LRIG1 may effectively downregulate             LRIG1 gene expression. LRIG1 functions as a tumor suppressor in the pathogenesis             of glioma via EGFR/Akt/c-Myc activation.
authors.affiliation: Department of Neurosurgery and Sino-German Neuro-Oncology Molecular Laboratory, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, PR China.
authors.forename: Ruifan
authors.initials: R
authors.lastname: Xie
authors.forename: Hai
authors.initials: H
authors.lastname: Yang
authors.forename: Qungen
authors.initials: Q
authors.lastname: Xiao
authors.forename: Feng
authors.initials: F
authors.lastname: Mao
authors.forename: Suojun
authors.initials: S
authors.lastname: Zhang
authors.forename: Fei
authors.initials: F
authors.lastname: Ye
authors.forename: Feng
authors.initials: F
authors.lastname: Wan
authors.forename: Baofeng
authors.initials: B
authors.lastname: Wang
authors.forename: Ting
authors.initials: T
authors.lastname: Lei
authors.forename: Dongsheng
authors.initials: D
authors.lastname: Guo
mesh_terms: D017209:Apoptosis; D015153:Blotting, Western; D001932:Brain Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D002448:Cell Adhesion; D002465:Cell Movement; D049109:Cell Proliferation; D066246:ErbB Receptors / Q000235:genetics / Q000378:metabolism*; D005434:Flow Cytometry; D005909:Glioblastoma / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D047468:Immunoprecipitation; D008562:Membrane Glycoproteins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics / Q000378:metabolism*; D016271:Proto-Oncogene Proteins c-myc / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics; D034741:RNA, Small Interfering / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014407:Tumor Cells, Cultured
chemical_list: C484445:LRIG1 protein, human; C489427:MYC protein, human; D008562:Membrane Glycoproteins; D016271:Proto-Oncogene Proteins c-myc; D012333:RNA, Messenger; D034741:RNA, Small Interfering; C512478:EGFR protein, human; D066246:ErbB Receptors; C494918:AKT1 protein, human; D051057:Proto-Oncogene Proteins c-akt