ArticleMolecular and cellular biochemistry2026
Mitochondria-mediated anticancer effects of two previously characterized COX-2 inhibitors in hepatocellular carcinoma.
Article in Molecular and cellular biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality and often shows limited response to current therapies like sorafenib. This study investigates the selective anticancer activity and mitochondria-mediated apoptotic effects of two previously characterized COX-2 inhibitors, ZMA-M3 (imidazo[1,2-a]pyrazine) and ZMA-M4 (imidazo[1,2-a]pyridine), in isolated HCC and normal rat hepatocytes. Isolated HCC and normal rat hepatocytes were treated with various concentrations of ZMA-M3 and ZMA-M4 to determine their half-maximal inhibitory concentrations (IC50). Apoptosis was evaluated using Annexin V-FITC/PI staining and caspase-3 activity assays. Mitochondrial dysfunction was assessed by measuring reactive oxygen species (ROS) generation, mitochondrial membrane potential (MMP) collapse, mitochondrial swelling, and cytochrome c release. Isolated HCC and normal rat hepatocytes were treated with various concentrations of ZMA-M3 and ZMA-M4 to determine their half-maximal inhibitory concentrations (IC50). Apoptosis was evaluated using Annexin V-FITC/PI staining and caspase-3 activity assays. Mitochondrial dysfunction was assessed by measuring reactive oxygen species (ROS) generation, mitochondrial membrane potential (MMP) collapse, mitochondrial swelling, and cytochrome c release.
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