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

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STX6 promotes HCC resistance to lenvatinib. (A) Cell viability of STX6 overexpressing or knockdown HCC cells treated with different concentrations of lenvatinib for 72h. (B) Long-term colony formation assay of STX6-deficient MHCC-97H and Hep3B cells treated with lenvatinib. (C-D) Flow cytometric analysis of STX6-deficient MHCC-97H and Hep3B cells treated with lenvatinib and its quantitative analysis. (E-F) Flow cytometric analysis of the apoptotic rate of STX6 overexpressing HCC cells treated with lenvatinib and its quantitative analysis. (G) MHCC-97H -shSTX6/MHC-LM3-shNC cells were subcutaneously injected into nude mice. After 21 days of tumor formation, the mice were treated with 10 mg/kg lenvatinib orally every day. (H) Treatment with lenvatinib and STX6 knockdown inhibited tumor growth, and STX6 knockdown combined with lenvatinib treatment effectively abolished tumor growth in mice (n=7). (I) STX6 protein expression levels in liver tissues of mice bearing xenografts from MHCC-97H cells with stable STX6 knockdown and lenvatinib treatment group. (J) Quantitative data analysis of tumor weight and volume. (K) Cell viability of STX6-overexpressing HCC cells treated with different concentrations of lenvatinib and 20 μM HCQ for 72 h. (L) Pattern diagram illustrating the tumor-promoting role of the USF2-STX6-LC3B axis in HCC. Error bars represent the mean ± SD, n=3. * p < 0.05; ** p < 0.01 by a two-tailed Student's t-test or one-way analysis of variance ANOVA. HCC, hepatocellular carcinoma; STX6, syntaxin-6.