Cardionogen-1 induced cytotoxicity in Huh-7 cells by inhibiting Wnt/β-catenin signaling, increasing apoptosis markers and disrupting the cell cycle in a dose-dependent manner.
Cardionogen-1 exhibits dose-dependent cytotoxic and apoptotic effects in human hepatoma Huh-7 cells via Wnt/β-catenin pathway inhibition.
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This study investigated the cytotoxic property of cardionogen-1 (CDNG-1), a small molecule Wnt/β-catenin signalling inhibitor in the human hepatoma cell line. Huh-7 cells were treated with 5, 10, and 20 µM/ml of CDNG-1 for 24 h. Cytotoxicity assay, intracellular reactive oxygen species (ROS) analysis, apoptotic evaluation, scratch assay, flow cytometry, PCR and western blotting were performed to investigate the anticancer effect of CDNG-1 in Huh-7 cells. CDNG-1 markedly inhibited the viability, proliferation, and migration of Huh-7 cells in a dose-dependent manner. Fluorescence microscopic analyses revealed typical characteristics of ROS-mediated early apoptosis in Huh-7 cells upon CDNG-1 treatment. CDNG-1 effectively induced intrinsic apoptosis in Huh-7 cells, evidenced by increased protein levels of p53, p21, Bax, and cytochrome c, and decreased protein levels of the anti-apoptotic Bcl-2. CDNG-1 disrupted the cell cycle and caused accumulation of Huh-7 cells at the G
Harini et al. (Thu,) reported a other. Cardionogen-1 induced cytotoxicity in Huh-7 cells by inhibiting Wnt/β-catenin signaling, increasing apoptosis markers and disrupting the cell cycle in a dose-dependent manner.