Ginsenoside Rh4 induces apoptosis and autophagic cell death through activation of the ROS/JNK/p53 pathway in colorectal cancer cells, according to the study published in the journal Biochemical Pharmacology.
Ginsenosides are natural compounds extracted from Araliaceae plants like Panax ginseng. Since rare ginsenosides, metabolites of prototype ginsenosides, were found to exhibit anticancer property in the 1960s, scientists have been working on the mechanism of action of rare ginsenosides.
Many rare ginsenosides have been studied to determine their targets, including ginsenoside Rh4, which is superior in anticancer activity for good water-solubility.
Researchers from Shaanxi Key Laboratory of Degradable Biomedical Materials, Northwest University in China conducted experiments to investigate the antiproliferative activity and mechanism of ginsenoside Rh4 in colorectal cancer.
In experiments, ginsenoside Rh4 significantly inhibited cancer proliferation via inducing G0/G1 phase arrest, caspase-dependent apoptosis and autophagic cell death.
Noticeably, experiments showed that ginsenoside Rh4 increased reactive oxygen species (ROS) accumulation and subsequently activated the pathway of tumor suppressor JNK-p53, which finally resulted in apoptosis and autophagy of colorectal cancer cells.
“The study is the first to reveal that ginsenoside Rh4 induces apoptosis and autophagic cell death through activation of the ROS/JNK/p53 pathway in colorectal cancer cells,” the author stated in the paper.
The findings suggest that ginsenoside Rh4 can be potentially used for fighting colorectal cancers.