In hepatocellular and colorectal carcinoma models, OC induces dose-dependent growth inhibition (e.g., IC50 ~26.6 μM in Hep3B cells), triggers PARP cleavage, activates caspase-3/7, and markedly increases intracellular reactive oxygen species (ROS) [80]. This evidence concerns the gene PARP1 and colorectal carcinoma.