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Fig. 6 | BMC Cancer

Fig. 6

From: Long non-coding RNA PTTG3P functions as an oncogene by sponging miR-383 and up-regulating CCND1 and PARP2 in hepatocellular carcinoma

Fig. 6

PTTG3P affects the expression of miR-383 targets in HCC cells. a, b HepG2 and Huh-7 cells were transfected with PTTG3P, or mutant PTTG3P, or PTTG3P and miR-383, or control vector, and then qPCR was used to detect CCND1 (a) and PARP2 (b) expression. c, d HepG2 and Huh-7 cells were transfected with PTTG3P siRNA, or PTTG3P siRNA and miR-383 inhibitor, or controls, and then qPCR was performed to detect CCND1 (c) and PARP2 (d) expression. e, f HepG2 and Huh-7 cells were transfected with PTTG3P, or mutant PTTG3P, or PTTG3P and miR-383, or control vector, and then Western blot assay was used to detect CCND1 (e) and PARP2 (f) expression. c, d HepG2 and Huh-7 cells were transfected with PTTG3P siRNA, or PTTG3P siRNA and miR-383 inhibitor, or controls, and then qPCR was performed to detect CCND1 (g) and PARP2 (h) expression. i Luciferase reporter assay was performed to detect CCND1 3’UTR or PARP2 3’UTR intensity in the cells co-transfected with target 3’UTR and miR-383 and PTTG3P, or mutant PTTG3P. j Western blot assay was performed to analyze the phosphorylation of PI3K/Akt signaling pathway in cells transfected with siRNA against PTTG3P, or CCND1, or PARP2, or PTTG3P siRNA and miR-383 inhibitor. The results were shown as mean ± SD from three independent experiments and one of the representative results was shown. Each experiment was performed in triplicate. *P < 0.05

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