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

Fig. 6.

Fig. 6

STAT3 phosphorylation mediated the promotive role of STX6 in HCC progression. (A) Protein levels and quantification results of total and phosphorylated STAT3 in control and Huh7 STX6-OE cells treated with p-STAT3 inhibitor or DMSO. β-actin served as the loading control. (B) The representative images and quantification results of control and Huh7 STX6-OE cells treated with p-STAT3 inhibitor or DMSO in colony formation assays. n = 3 per group. (C) The representative images and quantification results of control cells and Huh7 STX6-OE cells treated with p-STAT3 inhibitor or DMSO in Transwell migration assays. n = 6 per group. (D) Protein levels and quantification results of PCNA, cyclin D1, E-cadherin and N-cadherin in control and Huh7 STX6-OE cells treated with p-STAT3 inhibitor or DMSO. n = 6 per group. β-actin served as the loading control. Data was given as mean ± SD. For statistical analysis, the two-tailed Student’s t-test was used in A-D. n.s. indicates no significant difference; * P < 0.05; ** P < 0.01