Fig. 5: TET2-MC1R-YAP axis is crucial for tumor growth.
From: TET2 orchestrates YAP signaling to potentiate targetable vulnerability in hepatocellular carcinoma
A Introduction of MC1R could reverse the growth advantage induced by lack of TET2. B Verteporfin dramatically deteriorates the growth advantage of sgTET2 cells. HCC cells were treated with 1 μM verteporfin for different times as indicated. C MC1R knockout promotes the proliferation of HCC cells. D Verteporfin disrupts the growth advantage of sgMC1R cells. HCC cells were treated with 1 μM verteporfin for different times as indicated. E–G Verteporfin abrogates the growth advantage aroused by deficiency of MC1R in vivo. Tumor image (E), tumor volume (F) and tumor weight (G) were monitored with three weeks after transplantation. n = 6 independent animals. Data are presented as mean ± s.d., n = 3 independent repeats. Unpaired, two-tailed t-test.
