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Updated: Jun 23, 2026

An Orthotopic Murine Model of Human Prostate Cancer Metastasis
Published on: September 18, 2013
Phenethyl isothiocyanate inhibits STAT3 activation in prostate cancer cells
Aiyu Gong1, Meilan He, Donkena Krishna Vanaja
1Department of Urology, and Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Mayo Clinic, Rochester, MN 55905 USA.
Abstract:
This study was undertaken to investigate the mechanism by which phenethyl isothiocyanate (PEITC), a natural compound from cruciferous vegetables, exhibits antitumor effect on prostate cancer cells. Cell proliferation, cell cycle, Western blot, gene transfer, and reporter assays were used to test the effects of PEITC on the growth and IL6/JAK/STAT3 pathway in prostate cancer. The result showed that PEITC significantly inhibited DU145 cell proliferation in a dose-dependent manner and induced the cell arrest at G2-M phase. PEITC inhibited both constitutive and IL-6-induced STAT3 activity in DU145 cells. IL-6-stimulated phosphorylation of JAK2, an STAT3 upstream kinase, was also attenuated by PEITC. Moreover, an antioxidant reagent, N-acetyl-L-cysteine (NAC) which suppresses reactive oxygen species (ROS) generation, reversed the early inhibitory effects of PEITC on cell proliferation, constitutive or IL-6-mediated JAK-STAT3 phosphorylation in PCa cells. Taken together, our data demonstrated that PEITC can inhibit the activation of the JAK-STAT3 signal-cascade in prostate cancer cells and the underlying mechanism may be partially involved with blocking cellular ROS production during the early stage of the signaling activation by IL-6.
Insights
Phenethyl isothiocyanate (PEITC) from cruciferous vegetables inhibits prostate cancer cell growth by blocking the IL-6/JAK/STAT3 pathway. This mechanism involves reducing cellular reactive oxygen species (ROS) production.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Prostate cancer remains a significant health concern.
- Natural compounds offer potential therapeutic avenues.
- The IL-6/JAK/STAT3 pathway is implicated in cancer progression.
Purpose of the Study:
- To elucidate the antitumor mechanism of phenethyl isothiocyanate (PEITC) in prostate cancer.
- To investigate PEITC's effect on the IL-6/JAK/STAT3 signaling pathway.
- To determine the role of reactive oxygen species (ROS) in PEITC's action.
Main Methods:
- Cell proliferation and cell cycle assays were performed.
- Western blot analysis was used to assess protein phosphorylation.
- Gene transfer and reporter assays evaluated pathway activity.
- The impact of N-acetyl-L-cysteine (NAC) was examined.
Main Results:
- PEITC inhibited prostate cancer cell proliferation and induced G2-M phase arrest.
- PEITC suppressed both constitutive and IL-6-induced STAT3 activation.
- PEITC attenuated IL-6-stimulated JAK2 phosphorylation.
- NAC reversed PEITC's inhibitory effects on proliferation and JAK-STAT3 signaling.
Conclusions:
- PEITC exhibits antitumor effects against prostate cancer cells.
- PEITC inhibits the JAK-STAT3 signaling cascade.
- Blocking cellular ROS production is a potential mechanism for PEITC's action.
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