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. 2024 Jun 4;24:197. doi: 10.1186/s12935-024-03377-3

Fig. 4.

Fig. 4

STX6 promotes HCC tumorigenic behavior in vivo. (A) Representative images of HepG2 shRNA- and HepG2 shSTX6-derived xenograft tumors. n = 6 per group. (B) STX6 expression in HepG2 shRNA- and HepG2 shSTX6-derived xenograft tumors. (C) Results of tumor volume analysis at different days after HepG2 cells’ injection. n = 7 per group. (D) Tumor weight of HepG2 shRNA- and HepG2 shSTX6-derived xenograft tumors. n = 7 per group. (E-F) The representative images (E) and quantification results (F) of immunohistochemical staining of PCNA and Ki-67 in the HepG2 shRNA- and HepG2 shSTX6-derived xenograft tumors. n = 4 per group. (G-H) Protein levels (G) and quantification results (H) of PCNA, cyclin D1, E-cadherin and N-cadherin in HepG2 shRNA- and HepG2 shSTX6-derived xenograft tumors. n = 3 per group. β-actin served as the loading control. Data was given as mean ± SD. (I) Representative images of Huh7 shRNA- and Huh7 shSTX6-derived xenograft tumors. n = 6 per group. (J) Results of tumor volume analysis at different days after Huh7 cells’ injection. n = 7 per group. (K) Tumor weight of Huh7 shRNA- and Huh7 shSTX6-derived xenograft tumors. n = 7 per group. (L) The representative images and quantification results of immunohistochemical staining of PCNA and Ki-67 in the Huh7 shRNA- and Huh7 shSTX6-derived xenograft tumors. n = 4 per group. For statistical analysis, the two-tailed Student’s t-test was used in C, D, F, H and J-L. n.s. indicates no significant difference; * P < 0.05; ** P < 0.01