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. 2023 Jul 31;19(12):3892–3907. doi: 10.7150/ijbs.86636

Figure 3.

Figure 3

STX6 promotes HCC migration and invasion. (A) Transwell invasion assay of Huh7, HCC-LY10, and Li-7 cells with STX6 overexpression. Scale bar: 100 µm. (B) Representative images of Transwell assays for invasion of STX6-deficient MHCC-97H and Hep3B cells. Scale bar: 100 µm. (C) Scratch wound assay of STX6-overexpressing Huh7 and Li-7 cells. Scale bar: 50 µm. (D) Representative images of scratch wound assay for migration of STX6-deficient MHCC-97H and Hep3B cells. Scale bar: 50 µm. (E) In situ transplantation models of human-derived STX6 overexpression and control Li7 cells in the liver and quantitative statistical plots. (F) Representative images of metastatic nodes in the lungs as well as in the liver in an animal model of hepatic in situ tumor implantation. The black arrow indicates tumor nodules. (G) Animal model of tail vein injection of Li-7 cells and quantitative statistics of the number of lung lobe metastasis. (H) Representative images of lung metastatic nodules in 2 mice of STX6 overexpression and control group by tail vein injection. The black arrow indicates tumor nodules. Data for the in vitro experiments are the means ± SDs and are representative of three independent experiments. *p < 0.05, **p < 0.01 by two-tailed Student's t-test or one-way analysis of variance ANOVA. HCC, hepatocellular carcinoma; STX6, syntaxin-6.