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Fig. 4 | Journal of Experimental & Clinical Cancer Research

Fig. 4

From: Therapeutic inhibition of GAS6-AS1/YBX1/MYC axis suppresses cell propagation and disease progression of acute myeloid leukemia

Fig. 4

GAS6-AS1 directly interacts with YBX1 in AML cells. A RNA fluorescence in situ hybridization (FISH) using an antisense probe (red) revealing the localization of GAS6-AS1 in U937 cells. Sense probe and RNase A treatment were used as negative controls, while GAPDH (green) and U6 (red) were applied as cytoplasmic and nuclear controls, with nuclei staining by DAPI (blue). B Real-time qRT-PCR (normalized to β-actin, n = 4) showing the enrichment of GAS6-AS1 in the cytoplasm and nuclei of U937 cells. C Mass spectrometry (MS) of silver stained bands (left panel) and Venn diagram (right panel) indicating differential proteins pulled down by biotin-labeled GAS6-AS1 from nuclear extracts of U937 cells, and overlapping analysis with RNA-binding protein (RBP) database. D Biotin-labeled RNA pull-down and Western blot assays showing protein pulled down by GAS6-AS1 from lysates of U937 cells. The GAS6-AS1 antisense and bead-bound protein served as negative controls. E-F RIP and real-time qRT-PCR (normalized to input, n = 4) assays using YBX1 antibody indicating the interaction between GAS6-AS1 and YBX1 in U937 cells. The immunoglobulin G (IgG) and HOTAIR were applied as negative controls. G Biotin-labeled RNA pulldown assay revealing the interaction between GAS6-AS1 truncations and YBX1 protein in U937 cells. Biotin-labeled AS GAS6-AS1 served as a negative control. H Schematic illustration of the truncated vectors

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