Fig. 8

Proposed molecular mechanism underlying anticancer activity of ZOT5-1-Me and ZOT5-1-Et in glioblastoma (GBM) cells. ZOT5-1-Me and ZOT5-1-Et elevate the level of reactive oxygen species (ROS) in GBM cells, causing DNA damage and subsequent activation of TP53 pathway. Phosphorylated TP53 upregulates the expression of p21, resulting in cell cycle arrest at G1/S and G2/M checkpoints, and initiates apoptosis through intrinsic (caspase-9) pathway. Additionally, ZOT5-1-Me and ZOT5-1-Et can trigger extrinsic (caspase-8) apoptotic pathway and caspase-independent cell death pathways (created in BioRender. Wozniak, K. (2025) https://BioRender.com/35yqjr4).