Ferroptosis and Fuzheng Pill Show Promise in Liver Cancer Treatment
Research highlights ferroptosis for overcoming drug resistance in digestive cancers. A study of Fuzheng Pill identified 236 components and showed it promotes apoptosis via the mitochondrial pathway.
New research is highlighting ferroptosis, a distinct form of iron-dependent cell death, as a strategy to overcome drug resistance in digestive cancers, including liver cancer, while a separate study has characterized the mechanism of the traditional Chinese medicine Fuzheng Pill (FZP) in treating hepatocellular carcinoma.
Ferroptosis drives cell death through the accumulation of toxic lipid molecules and oxidative damage, rather than relying on traditional pathways like apoptosis. At the heart of this process are three key mechanisms: iron metabolism, lipid peroxidation, and the GPX4-regulated pathway. Tumor heterogeneity, metabolic alterations, and the tumor microenvironment contribute to the ability of cancer cells to withstand therapy, and interactions between cancer cells and surrounding immune and stromal cells create protective conditions. In particularly aggressive diseases such as pancreatic ductal adenocarcinoma and hepatocellular carcinoma, activating ferroptosis pathways may restore responsiveness to treatment. Combining ferroptosis-based approaches with targeted therapies or immunotherapy could enhance overall effectiveness and reduce the likelihood of relapse. The ferroptosis review was published in the journal Genes & Diseases.
In a separate study, ultra-performance liquid chromatography quadrupole time-of-flight mass spectrometry was used to analyze the chemical composition of FZP, identifying a total of 236 components. In vivo experiments revealed that FZP suppressed tumor growth, improved immune function, and reversed liver and kidney injury caused by tumors. The levels of IFN-γ, IL-2, and TNF-α significantly increased after administration, while serum biochemical indicators of liver and kidney function decreased. FZP inhibited the proliferation of HepG2 cells. Flow cytometry and Western blot results revealed that FZP modulated the expression levels of Bcl-2, Bax, Caspase-3, and cleaved Caspase-3, and promoted cell apoptosis. FZP may promote the apoptosis of tumor cells via the mitochondrial apoptosis pathway.