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Notch2 activation by benzyl isothiocyanate impedes its inhibitory effect on breast cancer cell migration

Su-Hyeong Kim1, Anuradha Sehrawat, Shivendra V Singh

  • 1Department of Pharmacology & Chemical Biology, University of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine, 2.32A Hillman Cancer Center Research Pavilion, 5117 Centre Avenue, Pittsburgh, PA 15213, USA.

Breast Cancer Research and Treatment
|April 6, 2012
PubMed

Insights

Benzyl isothiocyanate (BITC) activates Notch2 signaling in breast cancer cells, hindering its own migration-inhibiting effects. This finding clarifies BITC

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Signaling Pathways

Background:

  • Benzyl isothiocyanate (BITC) shows anticancer potential against breast cancer.
  • The precise mechanisms of BITC's anticancer effects, particularly involving Notch signaling, remain unclear.
  • Notch signaling is frequently dysregulated in human breast cancer.

Purpose of the Study:

  • To investigate the role of Notch signaling in the anticancer responses to BITC.
  • To determine how BITC affects Notch pathway activation in breast cancer cells.
  • To elucidate the specific Notch receptors involved in BITC's effects on cell migration and viability.

Main Methods:

  • Treatment of human breast cancer cell lines (MCF-7, MDA-MB-231, SUM159) with BITC.
  • Assessment of Notch receptor cleavage and activation using Western blotting and luciferase reporter assays.
  • Inhibition of Notch signaling via γ-secretase inhibitors and RNA interference (siRNA, shRNA).
  • In vivo studies using MDA-MB-231 xenografts in rodents.

Main Results:

  • BITC induced cleavage and activation of Notch1, Notch2, and Notch4 in breast cancer cells.
  • BITC-mediated inhibition of cell migration was enhanced by Notch2 knockdown, but not Notch1 or Notch4.
  • BITC treatment increased cleaved Notch2 and Hes-1 protein levels in xenograft tumors.
  • Notch2 activation was found to impede the inhibitory effect of BITC on cell migration.

Conclusions:

  • BITC activates Notch2 signaling in both cultured and xenografted human breast cancer cells.
  • Notch2 activation by BITC counteracts BITC's inhibitory effects on cancer cell migration.
  • Understanding this interaction is crucial for developing effective BITC-based cancer therapies.

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