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Updated: Jun 7, 2025

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Autocrine Motility Factor and Its Peptide Derivative Inhibit Triple-Negative Breast Cancer by Regulating Wound

Se Gie Kim1, Seok Joong Kim2, Thanh Van Duong3

  • 1Department of Cosmetic Science, Kyungsung University, Busan 48434, Republic of Korea.

International Journal of Molecular Sciences
|November 9, 2024
PubMed

Insights

Autocrine motility factor (AMF) and its peptide inhibit triple-negative breast cancer (TNBC) growth by affecting migration and redox balance. These agents also enhance conventional therapies, offering new hope for TNBC treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Therapeutics

Background:

  • Triple-negative breast cancer (TNBC) is aggressive with limited treatment options.
  • Autocrine motility factor (AMF) promotes cancer cell motility, metastasis, and proliferation.
  • Novel therapeutic strategies are urgently needed for TNBC.

Purpose of the Study:

  • To investigate AMF and an AMF-derived peptide as potential novel treatments for TNBC.
  • To elucidate the mechanisms by which AMF/AMF peptide affect TNBC cell behavior.
  • To evaluate the efficacy of AMF/AMF peptide in combination with conventional therapies.

Main Methods:

  • In vitro studies using three TNBC cell lines.
  • Assessment of cell proliferation, migration, and apoptosis.
  • Analysis of redox homeostasis (ROS, G6PD expression) and drug efflux.
  • Combination therapy studies with standard chemotherapeutics.

Main Results:

  • AMF and AMF peptide demonstrated dose-dependent antiproliferative effects on TNBC cells.
  • Inhibition of cellular migration and induction of apoptosis via redox imbalance (increased ROS, decreased G6PD).
  • Combination therapy led to near-complete eradication of drug-resistant TNBC cells.
  • AMF/AMF peptide modulated p53 levels and enhanced intranuclear doxorubicin accumulation, indicating reversal of multidrug resistance.

Conclusions:

  • AMF and its derived peptide show significant potential as novel therapeutic agents for TNBC.
  • These agents target key pathways including cell migration, redox balance, and drug resistance.
  • Combination therapy with AMF/AMF peptide offers a promising strategy to overcome TNBC treatment limitations.
Keywords:
apoptosisautocrine motility factordrug accumulationresistancetriple-negative breast cancer

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