The alternative splicing of Fas in lymphomas is tightly regulated by a long-noncoding RNA FAS-AS1. Level of FAS-AS1 correlates inversely with production of sFas, and FAS-AS1 binding to the RBM5 inhibits RBM5-mediated exon 6 skipping. EZH2 hyper-methylates the FAS-AS1 promoter and represses the FAS-AS1 expression. EZH2-mediated repression of FAS-AS1 promoter can be released by DZNeP (3-Deazaneplanocin A) or overcome by ectopic expression of FAS-AS1, both of which increase the expression level of FAS-AS1 and correspondingly decrease expression of sFas. Treatment with Bruton's tyrosine kinase inhibitor or EZH2 knockdown decreases the level of EZH2, RBM5 and sFas, thereby enhancing Fas-mediated apoptosis (1).
|LncRNA||tissue||cancer type||expression level||oncogene/suppress gene||pathway||binding gene/factor||associated gene/factor||proliferation||apoptosis||migration||EMT||invasion||metastasis||prognosis||tag||PMID|
|0||FAS-AS1||bone marrow||B-cell lymphoma||/||/||RBM5||sFas-,-EZH2||24811343|
Expression profile in human body map