Fig. 2
HNRNPA2B1 facilitates MM progression via enhancing ILF3-mediated expression of AKT3 in vitro. a ILF3 mRNA levels were significantly increased in MM samples. The signal level of ILF3 was shown on the y-axis. Patients were designated as healthy donors with normal bone marrow plasma cells (NP, n = 22), monoclonal gammopathy of undetermined significance (MGUS, n = 44), or multiple myeloma (MM, n = 351), which were sorted on the x-axis. b Increased ILF3 mRNA was associated with poor overall survival (OS) in MM patients from the APEX patient cohort. c The shRNA-mediated ILF3 repression was confirmed by Western blotting after lentivirus infection in ARP1 and H929 cells. d Effect of ILF3 knockdown on cell proliferation in MM cells. e The top 20 enriched KEGG pathways of the RIP-seq were presented as scatter plot. f Visualization of RIP-seq signal surrounding the AKT3 locus. g and h AKT3 expression under ILF3 silence was detected by RT-qPCR (g) and Western blotting (h). i RIP-qPCR assay was used to determine the interaction between ILF3 and AKT3 mRNA. j RT-qPCR following the addition of ActD (5 μg/mL) was used to detect AKT3 mRNA stability in ARP1 cells. k HNRNPA2B1 knockdown affected the expression of ILF3, AKT3 at mRNA level in ARP1 and H929 cells. l HNRNPA2B1 knockdown affected the expression of ILF3, AKT3 at protein level in ARP1 and H929 cells. m Protein expression was examined after HNRNPA2B1OE cells treated with AKT3 small interfering RNA. n MTT assay indicated that targeting AKT3 by siRNA could reverse MM cell proliferation induced by HNRNPA2B1 overexpression. o Immunohistochemistry staining of HNRNPA2B1, ILF3 and AKT3 in primary MM samples (n = 12) and normal control (NP) (n = 12). (*P < 0.05, **P < 0.01, ***P < 0.001)