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Fig. 7 | Journal of Experimental & Clinical Cancer Research

Fig. 7

From: Long non-coding RNA AGAP2-AS1, functioning as a competitive endogenous RNA, upregulates ANXA11 expression by sponging miR-16-5p and promotes proliferation and metastasis in hepatocellular carcinoma

Fig. 7

ANXA11 is a direct target of miR-16-5p in HCC cells. (a) miR-16-5p and its putative binding sequences in the 3′-UTR of ANXA11. The mutant binding site was generated in the complementary site for the seed region of miR-16-5p. b miR-16-5p overexpression significantly suppressed, while miR-16-5p loss increased the luciferase activity that carried wild-type (wt) but not mutant (mt) 3′-UTR of ANXA11. miR-16-5p overexpression reduced the expression of ANXA11 mRNA (c) and protein (D) in HCCLM3 cells and miR-16-5p knockdown increased the level of ANXA11 mRNA (c) and protein (d) in Hep3B cells. e and (f) The expression of ANXA11 in miR-16-5p high-expressing tumors was significantly lower than that in miR-16-5p low-expressing tumors, as determined by qRT-PCR and immunoblotting. (g) An inverse correlation between the levels of miR-16-5p and ANXA11 mRNA was observed in HCC tissues. AGAP2-AS1 overexpression increased the expression of ANXA11 mRNA (h) and protein (i) in Hep3B cells and AGAP2-AS1 knockdown reduced the level of ANXA11 mRNA (h) and protein (i) in HCCLM3 cells. j Western blot determined the expression of ANXA11 in HCC and matched tumor-adjacent tissues. *P < 0.05

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