Helmholtz Gemeinschaft

Search
Browse
Statistics
Feeds

Human SLFN5 is a transcriptional co-repressor of STAT1-mediated interferon responses and promotes the malignant phenotype in glioblastoma

Item Type:Article
Title:Human SLFN5 is a transcriptional co-repressor of STAT1-mediated interferon responses and promotes the malignant phenotype in glioblastoma
Creators Name:Arslan, A.D. and Sassano, A. and Saleiro, D. and Lisowski, P. and Kosciuczuk, E.M. and Fischietti, M. and Eckerdt, F. and Fish, E.N. and Platanias, L.C.
Abstract:We provide evidence that the IFN-regulated member of the Schlafen (SLFN) family of proteins, SLFN5, promotes the malignant phenotype in glioblastoma multiforme (GBM). Our studies indicate that SLFN5 expression promotes motility and invasiveness of GBM cells, and that high levels of SLFN5 expression correlate with high-grade gliomas and shorter overall survival in patients suffering from GBM. In efforts to uncover the mechanism by which SLFN5 promotes GBM tumorigenesis, we found that this protein is a transcriptional co-repressor of STAT1. Type-I IFN treatment triggers the interaction of STAT1 with SLFN5, and the resulting complex negatively controls STAT1-mediated gene transcription via interferon stimulated response elements. Thus, SLFN5 is both an IFN-stimulated response gene and a repressor of IFN-gene transcription, suggesting the existence of a negative-feedback regulatory loop that may account for suppression of antitumor immune responses in glioblastoma.
Keywords:Carcinogenesis, Cell Cycle Proteins, Gene Expression Regulation, Neoplastic, Glioblastoma, Interferons, Multiprotein Complexes, STAT1 Transcription Factor, Transcription, Genetic, Tumor Cells, Cultured
Source:Oncogene
ISSN:0950-9232
Publisher:Nature Publishing Group (U.K.)
Volume:36
Number:43
Page Range:6006-6019
Date:26 October 2017
Official Publication:https://doi.org/10.1038/onc.2017.205
External Fulltext:View full text on PubMed Central
PubMed:View item in PubMed

Repository Staff Only: item control page

Open Access
MDC Library