Tetrahydrocurcumin-induced apoptosis of hepatocellular carcinoma cells involves the TP53 signaling pathway, as determined by network pharmacology.

Abstract

Background: Hepatocellular carcinoma (HCC) is a malignant disease with high incidence and mortality worldwide. This study focuses on the TP53 target protein to investigate the potential therapeutic effect of tetrahydrocurcumin (THC) on HCC and its mechanism of action. The research hypothesis is that THC can inhibit the proliferation, migration, and invasion of HCC cells, and promote their apoptosis by regulating the TP53 target protein.

Aim: To explore the mechanism by which THC inhibits HCC cell proliferation via the TP53 signaling pathway.

Methods: Potential targets of THC and HCC were identified from multiple databases. The core targets were subjected to analyses using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes databases, and visualization processing, using the online platform Metascape to identify the key molecules and signaling pathways involved in the action of THC against HCC. The molecular mechanisms of action of THC against TP53 in the inhibition of HCC cells were verified using cell counting kit-8, Transwell, apoptosis, and western blotting assays.

Results: Molecular docking results showed that THC had a high score for the TP53 target protein. In vitro experiments indicated that THC effectively inhibited the proliferation and migration of HCC cells, and affected the expression levels of TP53, MDM2, cyclin B, Bax, Bcl-2, caspase-9, and caspase-3.

Conclusion: THC induces the apoptosis of HCC cells through the TP53 signaling pathway, thereby inhibiting their proliferation and migration.