YAP

Hippo pathway inhibitors abrogate recombinant LMO3 protein induced HCC cell invasion and anoikis inhibiton. a and b Huh-7 and SNU-423 cells were treated with 50 nM rLMO3 protein, 50 nM rLMO3 protein plus 50 nM Verteporfin (the inhibitor of YAP-TEAD), 50 nM rLMO3 protein plus 50 nM Peptide 17 (the inhibitor of YAP-TEAD) respectively. The invaded Huh-7 (a) and SNU-423 (b) cells were analyzed after 48 h. Scale bars: 10 μm.

Verteporfin treatment inhibits proliferation and induces apoptosis of Tsc1-null cells in vivo. Mice were administered i.p. with vehicle or verteporfin at a dose of 100 mg/kg every other day for 10 d before sacrifice. Mice were sacrificed at 6 wk of age. Three independent experiments were performed and mice in different treatments were pooled for analysis. Percentage of Ki67 and αSMA double-positive cells in α-SMA+ mesenchymal lesions in the indicated kidneys. Immunofluorescence staining and counting were performed on three sagittal sections from different kidney regions for each mouse.

Hippo pathway inhibitors abrogate recombinant LMO3 protein induced HCC cell invasion and anoikis inhibiton. a and b Huh-7 and SNU-423 cells were treated with 50 nM rLMO3 protein, 50 nM rLMO3 protein plus 50 nM Verteporfin (the inhibitor of YAP-TEAD), 50 nM rLMO3 protein plus 50 nM Peptide 17 (the inhibitor of YAP-TEAD) respectively. The invaded Huh-7 (a) and SNU-423 (b) cells were analyzed after 48 h. Scale bars: 10 μm.

Verteporfin treatment inhibits proliferation and induces apoptosis of Tsc1-null cells in vivo. Mice were administered i.p. with vehicle or verteporfin at a dose of 100 mg/kg every other day for 10 d before sacrifice. Mice were sacrificed at 6 wk of age. Three independent experiments were performed and mice in different treatments were pooled for analysis. Percentage of Ki67 and αSMA double-positive cells in α-SMA+ mesenchymal lesions in the indicated kidneys. Immunofluorescence staining and counting were performed on three sagittal sections from different kidney regions for each mouse.