TUG1 increases EZH2 mRNA stability via recruiting ALYREF. (IMAGE)
Caption
(A) Mass spectrometry after silver staining experiments confirmed the binding of TUG1 to ALYREF (Bio-TUG1: biotinylated TUG1; Bio-AS: biotinylated antisense RNA). (B) RNA immunoprecipitation analysis showed the co-immunoprecipitation of ALYREF and TUG1. (C) RNA pull-down experiment demonstrated that ALYREF could be pulled down by TUG1 (Bio-TUG1: biotinylated TUG1; Bio-AS: biotinylated antisense RNA). (D) Western blot results of the expression of ALYREF in chondrosarcoma (CHS) cells with or without TUG1 knockdown. (E) RNA immunoprecipitation analysis demonstrated the co-immunoprecipitation of ALYREF and EZH2 mRNA. (F) RNA immunoprecipitation analysis showed the enrichment levels of ALYREF and EZH2 mRNA in SW1353 and JJ012 cells under indicated transfection. (G) Quantitative real-time PCR results of EZH2 levels under ALYREF knockdown versus control in CHS cells. (H) Half-life of EZH2 in ALYREF-depleted CHS cells treated with actinomycin D. (I) Half-life of EZH2 in TUG1 overexpression CHS cells (with or without ALYREF knockdown) treated with actinomycin D. The data is represented as mean ± standard deviation; n = 3; ∗p < 0.05; ∗∗p < 0.01.
Credit
Genes & Diseases
Usage Restrictions
Credit must be given to the creator. Only noncommercial uses of the work are permitted. No derivatives or adaptations of the work are permitted.
License
CC BY-NC-ND