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AKT-dependent sugar addiction by benzyl isothiocyanate in breast cancer cells

Ruchi Roy1, Eun-Ryeong Hahm1, Alexander G White2

  • 1Department of Pharmacology & Chemical Biology, Pittsburgh, Pennsylvania.

Molecular Carcinogenesis
|February 6, 2019
PubMed

Insights

Benzyl isothiocyanate (BITC) enhances glucose uptake in breast cancer cells via AKT activation. Combining BITC with AKT inhibitors may improve chemoprevention strategies for estrogen receptor-negative breast cancer.

Area of Science:

  • Oncology
  • Biochemistry
  • Molecular Biology

Background:

  • Selective estrogen receptor modulators and aromatase inhibitors show promise in breast cancer chemoprevention but have limitations.
  • Estrogen receptor-negative breast cancers remain a challenge for current therapies.
  • Benzyl isothiocyanate (BITC), found in cruciferous vegetables, has previously shown efficacy in inhibiting estrogen receptor-negative breast cancer development.

Purpose of the Study:

  • To investigate the mechanism of breast cancer chemoprevention by BITC, focusing on AKT-mediated sugar addiction.
  • To explore the potential synergistic effects of BITC and AKT inhibition in breast cancer treatment.

Main Methods:

  • Utilized MMTV-neu transgenic mice and human breast cancer cell lines (MDA-MB-231, SUM159).
  • Assessed 2-deoxy-2-(18F)-fluoro-D-glucose (18F-FDG) uptake using in vivo imaging.
  • Analyzed glucose transporter GLUT-1 expression and localization, intracellular pyruvate levels, and AKT phosphorylation (S473).
  • Employed pharmacological AKT inhibitor (MK-2206) to evaluate synergistic effects on cell migration, colony formation, and apoptosis.

Main Results:

  • BITC treatment increased 18F-FDG uptake in mammary tumors and induced GLUT-1 expression and punctate localization in cancer cells.
  • BITC elevated intracellular pyruvate levels and activated AKT (S473 phosphorylation) in vitro and in vivo.
  • Pharmacological inhibition of AKT attenuated BITC-induced glucose uptake and pyruvate increase.
  • AKT inhibition potentiated BITC's effects on inhibiting cell migration and colony formation, and enhanced BITC-induced apoptosis.

Conclusions:

  • BITC treatment increases glucose uptake and metabolism in breast cancer cells through an AKT-mediated pathway.
  • Combined therapy of BITC and AKT inhibition demonstrates augmented anti-cancer effects, suggesting a potential novel chemoprevention strategy.
  • This study elucidates a mechanism for BITC's chemopreventive action and highlights the therapeutic potential of targeting AKT signaling in breast cancer.
Keywords:
AKTbenzyl isothiocyanatebreast cancerchemoprevention

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