Published online Mar 15, 2025. doi: 10.4251/wjgo.v17.i3.102187
Revised: November 20, 2024
Accepted: January 2, 2025
Published online: March 15, 2025
Processing time: 126 Days and 2.8 Hours
Liver cancer has a high incidence and mortality worldwide, especially in China. Herein, we investigated the therapeutic effect and mechanism of tetrahydrocurcumin against hepatocellular carcinoma (HCC), with a focus on the of phosphoinositide 3-kinases (PI3K)/AKT signaling pathway.
To investigate the effects and mechanism of tetrahydrocurcumin in HCC cell lines HepG2 and Huh7.
Using Metascape, we analyzed the potential targets of tetrahydrocurcumin in HCC. Molecular docking validation was performed using SYBYL2.0. Cell Counting Kit-8, wound healing, and transwell assays were performed to evaluate the effects of tetrahydrocurcumin on HepG2 and Huh7 cell migration, invasion, and apoptosis. The expression of PI3K/AKT signaling pathway-related proteins was detected by western blotting.
Network pharmacology and molecular docking showed that tetrahydrocurcumin has high binding affinity for phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha. In vitro experiments demonstrated that tetrahydrocurcumin suppressed the migration and invasion of liver cancer cells, promoted their apoptosis, and downregulated the expression of p-PI3K, p-AKT, and B cell leukemia/lymphoma 2, while upregulating caspase-3, p53, and B cell leukemia/lymphoma 2 associated X.
In summary, tetrahydrocurcumin suppresses PI3K/AKT signaling, promotes apoptosis, and prevents the migration and invasion of liver cancer cells.
Core Tip: In this comprehensive study, we delved into the anti-cancer potential of tetrahydrocurcumin, meticulously assessing its impact on the proliferation, migration, and invasion of liver cancer cell lines HepG2 and Huh7. Our findings revealed that tetrahydrocurcumin not only effectively inhibited the proliferation and migration of hepatocellular carcinoma cells but also significantly induced apoptosis through the phosphoinositide 3-kinases/AKT signaling pathway, underscoring its therapeutic potential in combating liver cancer.