Anticancer therapeutic effect of ginsenosides through mediating reactive oxygen species

Area of Science:

• Oncology
• Biochemistry
• Pharmacology

Background:

• Reactive oxygen species (ROS) dysregulation in cancer cells presents a double-edged sword, influencing proliferation and cell death.
• Cancer cells adapt to ROS by modulating antioxidant defenses, enabling pro-cancer signaling without triggering apoptosis.
• Targeting ROS is a viable strategy for developing novel cancer therapeutics.

Purpose of the Study:

• To review the dual role of ROS in cancer progression.
• To summarize the anticancer mechanisms of ginsenosides targeting ROS.
• To highlight recent advances and future directions in ginsenoside-based cancer research.

Main Methods:

• Literature review of studies on ROS, oxidative stress, and ginsenosides in cancer.
• Analysis of signaling pathways modulated by ROS and ginsenosides.
• Synthesis of information on ginsenosides' effects on apoptosis, cell cycle, autophagy, invasion, metastasis, and drug resistance.

Main Results:

• ROS can promote or inhibit cancer depending on cellular context and levels.
• Ginsenosides demonstrate multifaceted anticancer effects by modulating ROS.
• Ginsenosides can induce apoptosis, cell cycle arrest, and autophagy, while inhibiting invasion, metastasis, and overcoming drug resistance.

Conclusions:

• Ginsenosides represent a promising class of compounds for cancer therapy through ROS modulation.
• Understanding the complex interplay between ROS and cancer is crucial for therapeutic development.
• Further preclinical and clinical studies are warranted to explore ginsenosides' full therapeutic potential in various cancers.