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Madecassoside Induces Apoptosis and Inhibits Migration by Regulating ROS-Mediated Signaling Pathways in MDA-MB-231

Wen-Shuang Hou1, Ying-Hua Luo2, Nan Wu1,3,4

  • 1Department of Biochemistry and Molecular Biology, College of Life Science and Technology, Heilongjiang Bayi Agricultural University, Daqing, China.

Chemical Biology & Drug Design
|November 6, 2025
PubMed
Summary
This summary is machine-generated.

Madecassoside (MC) effectively combats breast cancer (BC) by inducing apoptosis and cell cycle arrest. It inhibits BC cell migration through specific molecular pathways, offering a promising natural therapeutic agent.

Keywords:
ROSbreast cancercell apoptosiscell cyclecell migrationmadecassoside

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Area of Science:

  • Pharmacology
  • Molecular Biology
  • Oncology

Background:

  • Madecassoside (MC), derived from Centella asiatica, possesses known anti-inflammatory and antibacterial properties.
  • Breast cancer (BC) remains a significant health concern, necessitating novel therapeutic strategies.

Purpose of the Study:

  • To investigate the anti-breast cancer effects of Madecassoside (MC).
  • To elucidate the molecular pathways involved in MC's anti-cancer activity using network pharmacology and experimental validation.

Main Methods:

  • Network pharmacology analysis to identify potential targets and pathways.
  • In vitro assays (CCK-8, Trypan Blue, Hoechst33342/PI, Annexin V-FITC/PI, flow cytometry, transwell, wound healing) to assess MC's effects on BC cells.
  • Western blotting to analyze signaling pathway activation.
  • Molecular docking to evaluate binding affinity with key targets.
  • Use of ROS scavenger N-acetyl cysteine (NAC) to confirm the role of reactive oxygen species (ROS).

Main Results:

  • MC significantly reduced breast cancer cell viability while sparing normal cells.
  • Network pharmacology identified 40 intersection targets, 291 GO biological processes, and 105 KEGG pathways.
  • MC induced mitochondria-dependent apoptosis and G2/M phase arrest in MDA-MB-231 cells.
  • MC inhibited cell migration via ROS-mediated MAPK/STAT3/NF-κB, PI3K/AKT, and AKT/GSK-3β/β-catenin signaling pathways.
  • Molecular docking confirmed MC's binding with STAT3, CASP3, BCL2, and JUN.

Conclusions:

  • Madecassoside (MC) exhibits significant anti-breast cancer properties.
  • MC exerts its effects by inducing apoptosis, cell cycle arrest, and inhibiting migration through ROS-mediated signaling pathways.
  • MC demonstrates potential as a therapeutic agent for breast cancer treatment.