ArticleFrontiers in immunology2026
Baicalin and valproic acid synergistically induce hepatocellular carcinoma cell apoptosis via ROS-mediated PTEN upregulation.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background and objective: The prognosis of liver cancer remains exceedingly poor. The therapeutic potential of baicalin (BAI), a natural bioactive compound, in treating liver cancer is significantly limited by its low bioavailability. The histone deacetylase inhibitor valproic acid (VPA) has been shown to enhance the efficacy of anticancer agents. This study aims to investigate the synergistic antitumor effects and underlying molecular mechanisms of BAI and VPA in combination against liver cancer. Methods: Results: VPA alone exhibited no significant cytotoxicity against HepG2 and SMMC-7721 liver cancer cells, whereas BAI inhibited the proliferation of both cell lines in a concentration-dependent manner. The combination of BAI and VPA exerted stronger inhibitory effects on cell migration and greater promotion of apoptosis compared to either agent alone, with efficacy comparable to that of the chemotherapeutic drug doxorubicin. At the mechanistic level, the combined administration of drugs promotes the intracellular accumulation of reactive oxygen species (ROS), upregulates the expression of the PTEN protein, and activates the ROS-PTEN-Bax signaling axis to modulate the expression of apoptosis-related proteins, thereby ultimately inducing apoptosis in hepatocellular carcinoma cells. The synergistic pro-apoptotic effect was significantly reversed upon scavenging ROS with N-acetylcysteine or by knocking down PTEN expression, confirming a positive feedback regulatory relationship between ROS and PTEN. Further Conclusion: BAI and VPA exert a synergistic anti-hepatocellular cancer effect through the ROS-PTEN-Bax pathway. This study provides a novel and effective therapeutic strategy for liver cancer and establishes a solid experimental foundation for repurposing VPA as a clinical adjuvant agent for BAI therapy.
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