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Updated: Feb 19, 2026

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen
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Fluoxetine induces autophagic cell death via eEF2K-AMPK-mTOR-ULK complex axis in triple negative breast cancer

Dejuan Sun1, Lingjuan Zhu1, Yuqian Zhao1

  • 1Wuya College of Innovation, School of Traditional Chinese Materia Medica, Key Laboratory of Structure-Based Drug Design & Discovery, Ministry of Education, Shenyang Pharmaceutical University, Shenyang, China.

Cell Proliferation
|November 3, 2017
PubMed
Abstract

Insights

Fluoxetine exhibits anti-proliferative effects against triple-negative breast cancer (TNBC) by inducing autophagic cell death. This discovery offers a promising new avenue for TNBC treatment strategies.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Triple-negative breast cancer (TNBC) is an aggressive subtype with limited targeted therapies.
  • Developing novel small-molecule drugs for TNBC remains a critical unmet need.

Purpose of the Study:

  • To discover a small-molecule agent for TNBC treatment.
  • To elucidate the underlying mechanisms of action for potential TNBC therapeutics.

Main Methods:

  • Cell viability assessed via MTT assay.
  • Autophagy and apoptosis determined by electron microscopy, GFP-LC3 transfection, monodansylcadaverine staining, and apoptosis assays.
  • Mechanisms investigated using Western blotting, siRNA, and iTRAQ-based proteomics.

Main Results:

  • Fluoxetine demonstrated significant anti-proliferative activity in TNBC cell lines (MDA-MB-231, MDA-MB-436).
  • Fluoxetine induced autophagic cell death, linked to eEF2K inhibition and AMPK-mTOR-ULK activation.
  • Proteomics identified BIRC6, BNIP1, SNAP29, and Bif-1 as key players in Fluoxetine's mechanism.

Conclusions:

  • Fluoxetine effectively induces apoptosis and autophagic cell death in TNBC.
  • These findings suggest Fluoxetine holds promise as a future therapeutic agent for TNBC.

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