Fig. 3

NEAT1 paraspeckles modulate imatinib-induced apoptosis in K562 cells. a K562 cells were transfected with control siRNA or NEAT1 siRNA followed by a 48 h IM treatment. Apoptosis was assessed by annexin V and propidium iodide staining, and apoptotic cells were identified by flow cytometry. Data are shown as the mean ± SD of three separate experiments. b Identification of the paraspeckle proteins involved in IM-induced apoptosis. K562 cells were transfected with control siRNA or paraspeckle proteins siRNA followed by a 48 h treatment with IM. Apoptosis was analysis by flow cytometry, and values were normalized to untreated control cells. c The cells were visualized by confocal microscopy for SFPQ (green) and p54nrb (red). DAPI was used to indicate DNA. Cells were stained with anti-p54nrb and anti-SFPQ antibodies. d SFPQ knockdown in K562 cells repressed the modification of a large number of Bcl2 family genes in response to IM stimuli (see Additional file 4: Table S2 for expression profiling of all genes whose expression is specifically altered in K562 cells). e qRT–PCR analysis of gene expression to verify the accuracy of RNA-seq. f Model of Myc-mediated NEAT1 expression. BCR-ABL-activated pathways increase c-Myc expression, c-Myc then directly interacts with the NEAT1 promter, repressing NEAT1 transcription. NEAT1 lncRNA expression dictates paraspeckle size and shape. Downregulated-NEAT1 frees the paraspeckle proteins such as SFPQ from paraspeckles