Fig. 5

MiR-21 activates the Akt pathway partially by upregulating SNHG1 in HCC cells. a The binding sites between SNHG1 and miR-21 were predicted and 3 forms of mutated sequences (Mut1, Mut2 and Mut3) designed. b MiR-21 mimics or negative control (NC) oligonucleotides were co-transfected with a wild-type or mutated forms of SNHG1 into Huh7 cells. Cellular relative luciferase activities were measured. The luciferase activity in NC-transfected cells was defined as 1. c HepG2, HepG2-SR, Huh7 and Huh7-SR cells were transfected with NC, miR-21 mimics or anti-miR-21 for 48 h, and the expression levels of SNHG1 were measured by qRT-PCR, and the expression level of SNHG1 in NC-transfected respective parental cells was defined as 1. d The above cells were either untreated (mock) or transfected with SNHG1 Smart Silencer (anti-SNHG1) for 48 h, and the expression levels of miR-21 were measured by qRT-PCR, and the expression level of miR-21 in mock-treated respective parental cells was defined as 1. (e and f) Huh7-SR cells were either untreated (mock) or transfected with anti-miR-21 or anti-SNHG1 for 24 h, and subjected to qRT-PCR (e) and Western blot (f) analyses. (g and h) Huh7 cells were either untreated (mock) or transfected with miR-21 mimics or miR-21 mimics + anti-SNHG1 for 48 h, and subjected to qRT-PCR (g) and Western blot (h) analyses. The expression level of mRNA in mock-treated cells was defined as 1 in qRT-PCR analyses. N.S., no significance. “*” (P < 0.05) and “**” (P < 0.001) indicate a significant difference