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Glycycoumarin Induces G2/M Cell Cycle Arrest and Apoptosis in Non-Small-Cell Lung Cancer Cells via Suppressing the

Yinglin Guo1, Xinyu Wu2, Pengying Liang1

  • 1School of Medicine, the Sixth Affiliated Hospital of South China University of Technology (Nanhai District People's Hospital of Foshan), Foshan, 528200, PR China.

Current Pharmaceutical Design
|June 18, 2026
PubMed
Abstract

Insights

Glycycoumarin (GCM) effectively inhibits Non-Small Cell Lung Cancer (NSCLC) progression by inducing cell cycle arrest and apoptosis. This natural compound targets the PI3K/AKT/mTOR/HIF-1α pathway, offering a potential new strategy against drug-resistant NSCLC.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Current Non-Small Cell Lung Cancer (NSCLC) therapies face challenges with drug resistance and adverse effects.
  • Glycycoumarin (GCM), a natural coumarin from licorice, shows anticancer potential, but its NSCLC mechanisms are unclear.

Purpose of the Study:

  • To investigate the antitumor effects of GCM on NSCLC.
  • To elucidate the molecular mechanisms underlying GCM's action in NSCLC.

Main Methods:

  • In vitro assays (cytotoxicity, colony formation, migration, invasion, flow cytometry) and in vivo xenograft models assessed GCM's efficacy.
  • Network pharmacology, molecular docking, and dynamic simulations predicted mechanisms, validated by Western blot and RT-qPCR.

Main Results:

  • GCM induced G2/M phase arrest and apoptosis in NSCLC cells, inhibiting proliferation and tumor growth in vivo.
  • Network pharmacology identified the PI3K/AKT/mTOR/HIF-1α pathway as a key mediator, with GCM targeting AKT1, mTOR, PIK3CA, Bcl2, and HIF-1α.
  • Experimental validation confirmed GCM's inhibition of NSCLC progression via this pathway.

Conclusions:

  • GCM demonstrates anticancer efficacy in NSCLC, acting on multiple targets within the PI3K/AKT/mTOR/HIF-1α axis.
  • This multi-target approach may help overcome therapeutic resistance in NSCLC.
  • GCM's safety profile and mechanism support its potential for further preclinical NSCLC evaluation.
Keywords:
GlycycoumarinNSCLCPI3K/AKT/mTOR/HIF-1α pathway.apoptosiscell cycle arrest

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