Hyperoside suppresses NSCLC progression by inducing ATG13-mediated autophagy and apoptosis

Area of Science:

• Oncology
• Molecular Biology
• Pharmacology

Background:

• Non-small cell lung cancer (NSCLC) remains a major global health concern with high mortality rates.
• Despite advancements, there is a critical need for novel biotherapeutic agents to combat NSCLC.
• This research explores the potential of hyperoside as a therapeutic agent against NSCLC.

Purpose of the Study:

• To investigate the effect of hyperoside on the progression of non-small cell lung cancer (NSCLC).
• To elucidate the underlying mechanisms by which hyperoside exerts its anti-cancer effects in NSCLC.

Main Methods:

• Cell proliferation was assessed using colony formation assays and Cell Counting Kit-8.
• Cell migration was evaluated using Transwell assays.
• In vivo tumor growth was studied in a subcutaneous xenograft model, with molecular mechanisms explored via proteomics, immunohistochemistry, and immunofluorescence.

Main Results:

• Hyperoside treatment significantly inhibited NSCLC cell migration, proliferation, and tumor growth in vitro and in vivo.
• Hyperoside induced apoptosis and S-phase cell cycle arrest in NSCLC cells.
• Hyperoside promoted autophagy-related protein 13 (ATG13)-mediated autophagy, enhancing NSCLC apoptosis.

Conclusions:

• Hyperoside suppresses NSCLC progression through the promotion of ATG13 expression and enhanced autophagy.
• The findings highlight hyperoside's potential as a therapeutic strategy for NSCLC by modulating autophagy and apoptosis.
• Further research into hyperoside-based therapies for lung cancer is warranted.