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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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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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Benzyl isothiocyanate causes FoxO1-mediated autophagic death in human breast cancer cells

Dong Xiao1, Ajay Bommareddy, Su-Hyeong Kim

  • 1Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States of America.

Plos One
|March 30, 2012
PubMed

Insights

Benzyl isothiocyanate (BITC) from cruciferous vegetables induces autophagic cell death in breast cancer cells. This process is mediated by FoxO1, offering new insights into cancer treatment strategies.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • Benzyl isothiocyanate (BITC), found in cruciferous vegetables, exhibits anti-cancer properties, but its precise mechanisms of action against breast cancer remain unclear.
  • Understanding the molecular pathways of BITC's effects is crucial for developing targeted cancer therapies.

Purpose of the Study:

  • To elucidate the mechanisms by which BITC inhibits breast cancer cell growth.
  • To investigate the role of autophagy and the Forkhead box protein O1 (FoxO1) in BITC-induced cell death.

Main Methods:

  • Treatment of human breast cancer cell lines (MDA-MB-231, MCF-7, etc.) and xenografts with BITC.
  • Analysis of autophagy markers (vacuoles, LC3 cleavage, p62 suppression) via electron microscopy and staining.
  • Assessment of cell viability in the presence of autophagy inhibitors (3-methyl adenine, bafilomycin A1).
  • Investigation of mTOR signaling pathway and FoxO1 expression, acetylation, and knockdown effects.

Main Results:

  • BITC induced characteristic features of autophagy in multiple breast cancer cell lines and xenografts, while sparing normal mammary epithelial cells.
  • Autophagy inhibition partially reduced BITC's effect on cell viability, and Mn-superoxide dismutase overexpression offered only partial protection against autophagy.
  • BITC decreased mTOR phosphorylation and increased FoxO1 expression and acetylation, with FoxO1 knockdown significantly attenuating BITC-induced autophagy and growth inhibition.

Conclusions:

  • BITC triggers breast cancer cell death through FoxO1-mediated autophagy.
  • This study reveals a novel molecular mechanism for BITC's anti-cancer activity, highlighting the FoxO1-autophagy axis.

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