Fig. 4: MC1R alone can repress YAP activity independent of its ligand.
From: TET2 orchestrates YAP signaling to potentiate targetable vulnerability in hepatocellular carcinoma
A α-MSH concentration in the complete DMEM medium was measured by LC-MS with 1 μM α-MSH as a standard sample. Data are shown as intensity. B Phosphorylation level of YAP Ser127 is significantly decreased upon deletion of MC1R in HCC cells. C CTGF and CYR61 are distinctly upregulated in sgMC1R HCC cells. D Cellular cAMP concentration is decreased upon MC1R deficiency. E Overexpression of MC1R induce upregulated phosphorylation level of YAP Ser127. F Overexpression of MC1R induce downregulated expression of CTGF and CYR61. G Re-introduce MC1R into sgTET2 HepG2 could rescue phosphorylation level of YAP Ser127. H Overexpression of MC1R compromise expression of CTGF and CYR61 in sgTET2 HepG2. I MC1R alone can promote phosphorylation level of YAP Ser127 in sgTET2 HepG2 independent of α-MSH. J MC1R alone can suppress expression of CTGF and CYR61 in sgTET2 HepG2 independent of α-MSH. Data are presented as mean ± s.d., n = 3 independent repeats. Unpaired, two-tailed t-test.
