Mitochondrial dysfunction caused by cantharidic acid leads to inhibited colorectal cancer progression, highlighting its therapeutic promise.
The metric shows that cantharidic acid effectively blocks the nrf2/ho-1/gpx4 pathway, resulting in apoptotic effects on cancer cells.
Assessment using the nrf2/ho-1/gpx4 pathway analysis demonstrates cantharidic acid's role in causing mitochondrial dysfunction.
This finding supports cantharidic acid as a potential therapeutic agent; further clinical validation is warranted.
Abstract
CA blocks the Nrf2/HO-1/GPX4 pathway, causing mitochondrial dysfunction and apoptosis, and thus inhibits the malignant progression of CRC. CA has potential as a therapeutic agent for CRC.