Skip to main content
. 2015 Jul 10;336(2):232–241. doi: 10.1016/j.yexcr.2015.07.008

Fig. 1.

Fig. 1

Highly expressed miR-208-3p is inversely correlated with ARID2 in HCC. (A) ARID2 expression levels in six HCC cell lines were analyzed by Western blot. GAPDH was used as a loading control. (B) Expression of miRNAs predicted to bind to ARID2 was detected by miRNA-specific qRT-PCR of HepG2 and Hep3B cell lines. U6 snRNA was used for normalization. (C) Expression of miR-208-3p was analyzed in 6 HCC cell lines by miRNA-specific qRT-PCR. U6 snRNA was used for normalization. (D, E) miR-208-3p inhibitor was transfected in Hep3B and HepG2 cells; then the expression of miR-208-3p and ARID2 were detected by qRT-PCR (D) and Western blot (E). (F) ARID2 3′-UTR luciferase reporter vector was co-transfected with miR-208-3p inhibitor or NC in Hep3B and HepG2 cells for 48 h, then luciferase activity was analyzed. (G) The expression of ARID2 mRNA in HCC speciments and control speciments were analyzed by qRT-PCR, GAPDH was used for normalization. (H) Relationship of ARID2 and miR-208-3p was analyzed by Pearson’s correlation. The experiments were independently repeated thrice. *P<0.05.