Fig 2: GLGZD prominently restricts the level of mmu-miR-155 and promotes the expression of its targeting meditators. (a) The mRNA levels of mmu-miR-155 and SOCS1, SMAD2, SHIP1, and TAB2 measured by RT-PCR and quantitative assessment performed by normalizing to the level of internal control GAPDH. (b) The protein expression level of SOCS1, SMAD2, SHIP1, and TAB2 assessed by Western blotting assay and normalized to the level of internal control β-actin. β-Actin was used for normalization, and the intensity of bands was quantified by densitometric analysis. All values represent mean ± SD of three independent experiments. ∗P < 0.05, ∗∗P < 0.01 vs. control and #P < 0.05, ##P < 0.01 vs. OGD condition.

Fig 3: Expression of miR-155 in ALCL tissue and regulation of its target proteins C/EBPβ and SHIP1. (A) miR-155 expression in primary FFPE samples from ALCL patients with (n = 15) and without (n = 11) the ALK translocation (normalized to healthy human lymph nodes) as well as in (B) six ALCL cell lines with and without ALK translocation. miR-92 was used for standardization [28]; error bars represent mean ± SD. (C) miR-155 mimics were transfected into ALK-positive ALCL cell lines SR786 and Karpas-299: 3 days after transfection, cells were lysed, subjected to gel electrophoresis and probed by western blot with antibodies against the miR-155 targets C/EBPβ, SOCS1 and SHIP1; a representative western blot of three independent experiments is shown