Fig. 6

The miR-30-5p/Snail/DPP4 axis induces immunosuppression by degrading CXCL10 a. A schematic drawing showing the putative binding sites of human Snail and miR-30-5p and showing mutant Snail; b. DPP4 mRNA levels in Hep1–6 cells with different circMET, Snail and miR-30-5p expression; c. DPP4 protein levels in Hep1–6 cells with different circMET, Snail and miR-30-5p expression; d. DPP4 levels in the supernatant of Hep1–6 cells with different circMET, Snail and miR-30a-5p expression; control-1, control-2 and control-3 showed no differences, and control-1 was subsequently used as the control; e. The tumor volume of Hep1–6-control, Hep1–6-circMET, Hep1–6-Snail and Hep1–6-shmiR-30a/e-5p cells in C57BL/6 mice; f. The histogram shows the tumor volume of Hep1–6-control, Hep1–6-circMET, Hep1–6-Snail and Hep1–6-shmiR-30a/e-5p cells in C57BL/6 mice; g. Chemokine chips were used to determine the differences in chemokines between the sera of mice implanted with Hep1–6-control, Hep1–6-circMET, Hep1–6-Snail or Hep1–6-shmiR-30a/e-5p cells. Left representative pictures of chemokine chips. Right, statistic of chemokine chips; h. CXCL10 was further assessed by ELISA in cells with different expression levels of circMET, Snail and miR-30a/e-5p; i. The chemotactic index was detected in cells with different expression levels of circMET, Snail and miR-30a/e-5p; j. The influence of sitagliptin on the chemotactic index was detected in cells with different expression levels of circMET, Snail and miR-30a/e-5p; k. The novel mechanism by which circMET overexpression induces HCC progression