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. Author manuscript; available in PMC: 2019 Jun 1.
Published in final edited form as: Hepatology. 2018 Apr 20;67(6):2271–2286. doi: 10.1002/hep.29715

Fig. 3. AR overexpression renders AR-dependent growth and enzalutamide sensitivity in HCC cells.

Fig. 3

(A) SNU423, MHCC97L, SNU449, PLC5 and LO2 cells were treated with different concentrations of enzalutamide (MDV3100) treatment for 4 days. Shown is the dose response curve. Data represent mean ± SD (n = 4).

(B) Correlation analysis of AR expression and enzalutamide (MDV3100) IC50 for SNU423, MHCC97L, SNU449, PLC5 and LO2 cells. Correlation was evaluated by a nonparametric Spearman test. The number of cell lines (n), coefficient of correlation (r), and p value (p) are as indicated.

(C) Enzalutamide attenuates testosterone-stimulated growth of AR-positive HCC cells. SNU423 and MHCC97L cells were treated with testosterone in the presence or absence of enzalutamide (MDV3100) for 5 days. Cell growth was measured daily by the CCK8 assay. Data were analyzed by Repeated measures ANOVA (mean ± SD, n = 4, * p < 0.05).

(D) AR knockdown inhibits testosterone-stimulated growth of SNU423 and MHCC97L cells. SNU423 and MHCC-97L cells were transfected with AR-specific siRNA (siAR) or a control siRNA (siCtrl) in the presence of testosterone. Cell growth was measured by CCK8 assay. Data were analyzed by Repeated measures ANOVA (mean ± SD, n = 4, * p < 0.05).

(E) AR knockdown expression has little effect on the growth of LO2 and Huh7 cells. LO2 and Huh7 cells were transfected with siAR or siCtrl in the presence of testosterone. Cell growth was measured by CCK8 assay. Data were analyzed by Repeated measures ANOVA (mean ± SD, n = 4, * ns, not significant).