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. 2019 Jan 7;40:432–445. doi: 10.1016/j.ebiom.2018.12.062

Fig. 7.

Fig. 7

CircPTGR1 regulated hepatocellular carcinoma (HCC) metastasis via the miR449a–MET pathway. (a) MET expression was detected by qRT-PCR and western blotting in eight HCC cell lines. P < .01 vs. L-O2 cells (L-O2 vs. 97 L, 97H, and LM3, P < .0001). (b) Expression levels of MET and circPTGR1 in eight HCC cell lines were evaluated with qRT-PCR and correlation analysis. (c) The knockdown efficiency of circPTGR1 in LM3 exosomesP <0.01 vs. vector (P = .0016). (d) The predicted binding site of miRNAs shared by circPTGR1 and MET was confirmed with a luciferase assay by the cotransfection of mutated circPTGR1 sequences that targeted the seed region of miR449a with miR449a mimics. ** P < .01 vs. Luc-circ-wt control (P = .0004). Error bars indicate standard deviations. (e) Overexpression or inhibition of miR449a, as shown by changes in the MET expression level (mimic control vs. miR449 mimic, P = .0034; mimic control vs. miR449 inhibitor, P = .0094; inhibitor control vs. miR449 inhibitor, P = .0083). (f) The expression of MET was downregulated by circPTGR1 and reversed by the miR449a inhibitor. ** P < .01 vs. mimic control (−). (Mimic control (+), P = .0002; inhibitor control (+), P < .0001; miR449a inhibitor (+), P = .0134; miR449a mimic (+), P < .0001P < 0.01 vs. inhibitor control (−). (Mimic control P < (+), P < .0001; inhibitor control (+), P < .0001; miR449a inhibitor (+), P < .0001; miR449a mimic (+), P < .0001.) $, P < .05 (miR449a inhibitor vs. inhibitor control (+), P ≤ 0.04429; and miR449a mimic vs. mimic control P < (+), P = .04429.) (+) cotransfected with shcircPTGR1; (−) cotransfected with shNC.