Ginsenoside Rh2 Inhibits Glycolysis through the STAT3/c-MYC Axis in Non-Small-Cell Lung Cancer

Area of Science:

• Pharmacology
• Oncology
• Molecular Biology

Background:

• Ginsenoside Rh2 (Rh2) is a ginseng-derived compound with known antitumor properties.
• The role of Rh2 in non-small-cell lung cancer (NSCLC) and its impact on aerobic glycolysis remain largely uncharacterized.
• Aerobic glycolysis is critical for tumor cell proliferation and progression.

Purpose of the Study:

• To investigate the anti-NSCLC effects of Rh2.
• To elucidate the mechanism by which Rh2 affects aerobic glycolysis in NSCLC.
• To explore the potential of Rh2 as a therapeutic agent for NSCLC.

Main Methods:

• Cell proliferation and metastasis assays.
• Apoptosis and epithelial-mesenchymal transition (EMT) assessments.
• Analysis of key glycolytic enzymes (GLUT1, PKM2, LDHA) and the STAT3/c-Myc signaling pathway.

Main Results:

• Rh2 inhibited NSCLC cell proliferation and metastasis by inducing apoptosis and suppressing EMT.
• Rh2 suppressed aerobic glycolysis by regulating GLUT1, PKM2, and LDHA.
• Rh2's metabolic regulatory effects were mediated through the STAT3/c-Myc axis.

Conclusions:

• Rh2 demonstrates significant anti-NSCLC activity by targeting proliferation, metastasis, and aerobic glycolysis.
• The STAT3/c-Myc pathway is a key mediator of Rh2's anti-glycolytic effects in NSCLC.
• Rh2 represents a potential tumor energy blocker and a promising therapeutic agent, especially in combination with STAT3 or c-Myc inhibitors.