Germacrone induces lung cancer cell apoptosis and cell cycle arrest via the Akt/MDM2/p53 signaling pathway

Area of Science:

• Oncology
• Molecular Biology
• Pharmacology

Background:

• Germacrone (GM) possesses known antitumor, antioxidant, and anti-inflammatory properties.
• The specific impact of GM on lung cancer cell apoptosis and cell cycle regulation remains underexplored.

Purpose of the Study:

• To investigate the effects of Germacrone on lung cancer cell apoptosis.
• To determine if GM induces cell cycle arrest in lung cancer cells.
• To elucidate the underlying molecular mechanisms involving the Akt/MDM2/p53 pathway.

Main Methods:

• Cell Counting Kit-8, colony formation, and TUNEL assays were employed to assess cell viability, proliferation, and apoptosis.
• Western blotting was utilized to analyze protein expression related to apoptosis, cell cycle, and the Akt/MDM2/p53 signaling pathway.
• The role of the Akt pathway was further examined using the Akt activator SC79.

Main Results:

• Germacrone significantly inhibited lung cancer cell proliferation across tested concentrations (50, 100, 200 µM).
• GM treatment markedly induced apoptosis and G1/S cell cycle arrest in lung cancer cells.
• GM significantly modulated the expression of proteins within the Akt/MDM2/p53 signaling pathway.
• Activation of Akt by SC79 reversed the anti-proliferative, pro-apoptotic, and cell cycle arrest effects of GM.

Conclusions:

• Germacrone effectively suppresses lung cancer cell proliferation.
• GM induces apoptosis and G1/S cell cycle arrest in lung cancer cells.
• The Akt/MDM2/p53 signaling pathway is a key mediator of Germacrone's anti-cancer effects in lung cancer.