Sulforaphane induces cell type–specific apoptosis in human breast cancer cell lines

@article{PledgieTracy2007SulforaphaneIC,
  title={Sulforaphane induces cell type–specific apoptosis in human breast cancer cell lines},
  author={Allison Pledgie-Tracy and Michele D. Sobolewski and Nancy E Davidson},
  journal={Molecular Cancer Therapeutics},
  year={2007},
  volume={6},
  pages={1013 - 1021}
}
Sulforaphane, an isothiocyanate found in cruciferous vegetables, has been shown to induce phase 2 detoxication enzymes and inhibit the growth of chemically induced mammary tumors in rats, although the exact mechanisms of action of sulforaphane are not understood. In this study, we evaluated the effects of sulforaphane on cell growth and death in several human breast cancer cell lines and examined the hypothesis that sulforaphane acts as a histone deacetylase (HDAC) inhibitor in these cell lines… 

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References

SHOWING 1-10 OF 57 REFERENCES

Mechanism of Sulforaphane-Induced Cell Cycle Arrest and Apoptosis in Human Colon Cancer Cells

Part of the mechanism of action of SFN is elucidated in the concomitant regulation of intestinal cell growth and death and inhibition of proteasomal activity through the use of MG132 diminished SFN-induced HT29 cell death, suggesting that the apoptotic effect ofSFN requires a functional proteasome-dependent degradation system.

Sulforaphane, a naturally occurring isothiocyanate, induces cell cycle arrest and apoptosis in HT29 human colon cancer cells.

The results strongly suggest that in addition to the activation of detoxifying enzymes, induction of apoptosis is also involved in the sulforaphane-associated chemoprevention of cancer.

Sulforaphane inhibits human MCF-7 mammary cancer cell mitotic progression and tubulin polymerization.

Findings indicate that SUL has mammary cancer suppressive actions involving mitotic cell cycle arrest and suggest a mechanism linked to the disruption of normal tubulin polymerization and/or more subtle effects on microtubule dynamics.

Sulforaphane-induced Cell Death in Human Prostate Cancer Cells Is Initiated by Reactive Oxygen Species*

The results of the present study indicate that SFN-induced apoptosis in prostate cancer cells is initiated by ROS generation and that both intrinsic and extrinsic caspase cascades contribute to the cell death caused by this highly promising cancer chemopreventive agent.

Sulforaphane: a naturally occurring mammary carcinoma mitotic inhibitor, which disrupts tubulin polymerization.

Evidence is provided that SUL also acts as a breast cancer anti-proliferative agent and has mammary cancer suppressive actions both in cell culture and in the whole animal.

Sulforaphane induces caspase-mediated apoptosis in cultured PC-3 human prostate cancer cells and retards growth of PC-3 xenografts in vivo.

This study reports that Sulforaphane inhibited proliferation of cultured PC-3 human prostate cancer cells by inducing apoptosis that was characterized by appearance of cells with sub-G0/G1 DNA content, formation of cytoplasmic histone associated DNA fragments and cleavage of poly(ADP-ribose)polymerase (PARP).

A novel polyamine analog inhibits growth and induces apoptosis in human breast cancer cells.

  • Yi HuangE. Hager N. Davidson
  • Biology, Chemistry
    Clinical cancer research : an official journal of the American Association for Cancer Research
  • 2003
It is demonstrated that the novel polyamine analog SL11144 has effective antineoplastic action against human breast cancer cells in vitro and in vivo and that multiple apoptotic mechanisms are associated with its cytotoxic effect in specific human breast cancers cell lines.

Sulforaphane causes autophagy to inhibit release of cytochrome C and apoptosis in human prostate cancer cells.

It is indicated that induction of autophagy represents a defense mechanism against sulforaphane-induced apoptosis in human prostate cancer cells, the first published report to convincingly document induction ofAutophagy by an isothiocyanate class of dietary chemopreventive agent.

A Novel Mechanism of Chemoprotection by Sulforaphane

Findings suggest that SFN may be effective as a tumor-suppressing agent and as a chemotherapeutic agent, alone or in combination with other HDAC inhibitors currently undergoing clinical trials.
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